Posted on by Dr. Francis Collins
As a cardiac electrophysiologist, Deeptankar DeMazumder has worked for years with people at risk for sudden cardiac arrest (SCA). Despite the latest medical advances, less than 10 percent of individuals stricken with an SCA will survive this highly dangerous condition in which irregular heart rhythms, or arrhythmias, cause the heart suddenly to stop beating.
In his role as a physician, DeMazumder keeps a tight focus on the electrical activity in their hearts, doing his best to prevent this potentially fatal event. In his other role, as a scientist at the University of Cincinnati College of Medicine, DeMazumder is also driven by a life-saving aspiration: finding ways to identify at-risk individuals with much greater accuracy than currently possible—and to develop better ways of protecting them from SCAs. He recently received a 2020 NIH Director’s New Innovator Award to pursue one of his promising ideas.
SCAs happen without warning and can cause death within minutes. Poor heart function and abnormal heart rhythms are important risk factors, but it’s not possible today to predict reliably who will have an SCA. However, doctors already routinely capture a wealth of information in electrical signals from the heart using electrocardiograms (ECGs). They also frequently use electroencephalograms (EEGs) to capture electrical activity in the brain.
DeMazumder’s innovative leap is to look at these heart and brain signals jointly, as well as in new ways, during sleep. According to the physician-scientist, sleep is a good time to search for SCA signatures in the electrical crosstalk between the heart and the brain because many other aspects of brain activity quiet down. He also thinks it’s important to pay special attention to what happens to the body’s electrical signals during sleep because most sudden cardiac deaths happen early in the waking hours, for reasons that aren’t well understood.
He has promising preliminary evidence from both animal models and humans suggesting that signatures within heart and brain signals are unique predictors of sudden death, even in people who appear healthy . DeMazumder has already begun developing a set of artificial intelligence algorithms for jointly deciphering waveform signals from the heart, brain, and other body signals [2,3]. These new algorithms associate the waveform signals with a wealth of information available in electronic health records to improve upon the algorithm’s ability to predict catastrophic illness.
DeMazumder credits his curiosity about what he calls the “art and science of healing” to his early childhood experiences and his family’s dedication to community service in India. It taught him to appreciate the human condition, and he has integrated this life-long awareness into his Western medical training and his growing interest in computer science.
For centuries, humans have talked about how true flourishing needs both head and heart. In DeMazumder’s view, science is just beginning to understand the central role of heart-brain conversations in our health. As he continues to capture and interpret these conversations through his NIH-supported work, he hopes to find ways to identify individuals who don’t appear to have serious heart disease but may nevertheless be at high risk for SCA. In the meantime, he will continue to do all he can for the patients in his care.
 Mitochondrial ROS drive sudden cardiac death and chronic proteome remodeling in heart failure. Dey S, DeMazumder D, Sidor A, Foster DB, O’Rourke B. Circ Res. 2018;123(3):356-371.
 Entropy of cardiac repolarization predicts ventricular arrhythmias and mortality in patients receiving an implantable cardioverter-defibrillator for primary prevention of sudden death. DeMazumder D, Limpitikul WB, Dorante M, et al. Europace. 2016;18(12):1818-1828.
 Dynamic analysis of cardiac rhythms for discriminating atrial fibrillation from lethal ventricular arrhythmias. DeMazumder D, Lake DE, Cheng A, et al. Circ Arrhythm Electrophysiol. 2013;6(3):555-561.
Sudden Cardiac Arrest (National Heart, Lung, and Blood Institute/NIH)
Deeptankar DeMazumder (University of Cincinnati College of Medicine)
DeMazumder Project Information (NIH RePORTER)
NIH Director’s New Innovator Award (Common Fund)
NIH Support: National Heart, Lung, and Blood Institute; Common Fund
Posted on by Dr. Francis Collins
More than 3 million people around the world, now tragically including thousands every day in India, have lost their lives to severe COVID-19. Though incredible progress has been made in a little more than a year to develop effective vaccines, diagnostic tests, and treatments, there’s still much we don’t know about what precisely happens in the lungs and other parts of the body that leads to lethal outcomes.
Two recent studies in the journal Nature provide some of the most-detailed analyses yet about the effects on the human body of SARS-CoV-2, the coronavirus that causes COVID-19 [1,2]. The research shows that in people with advanced infections, SARS-CoV-2 often unleashes a devastating series of host events in the lungs prior to death. These events include runaway inflammation and rampant tissue destruction that the lungs cannot repair.
Both studies were supported by NIH. One comes from a team led by Benjamin Izar, Columbia University, New York. The other involves a group led by Aviv Regev, now at Genentech, and formerly at Broad Institute of MIT and Harvard, Cambridge, MA.
Each team analyzed samples of essential tissues gathered from COVID-19 patients shortly after their deaths. Izar’s team set up a rapid autopsy program to collect and freeze samples within hours of death. He and his team performed single-cell RNA sequencing on about 116,000 cells from the lung tissue of 19 men and women. Similarly, Regev’s team developed an autopsy biobank that included 420 total samples from 11 organ systems, which were used to generate multiple single-cell atlases of tissues from the lung, kidney, liver, and heart.
Izar’s team found that the lungs of people who died of COVID-19 were filled with immune cells called macrophages. While macrophages normally help to fight an infectious virus, they seemed in this case to produce a vicious cycle of severe inflammation that further damaged lung tissue. The researchers also discovered that the macrophages produced high levels of IL-1β, a type of small inflammatory protein called a cytokine. This suggests that drugs to reduce effects of IL-1β might have promise to control lung inflammation in the sickest patients.
As a person clears and recovers from a typical respiratory infection, such as the flu, the lung repairs the damage. But in severe COVID-19, both studies suggest this isn’t always possible. Not only does SARS-CoV-2 destroy cells within air sacs, called alveoli, that are essential for the exchange of oxygen and carbon dioxide, but the unchecked inflammation apparently also impairs remaining cells from repairing the damage. In fact, the lungs’ regenerative cells are suspended in a kind of reparative limbo, unable to complete the last steps needed to replace healthy alveolar tissue.
In both studies, the lung tissue also contained an unusually large number of fibroblast cells. Izar’s team went a step further to show increased numbers of a specific type of pathological fibroblast, which likely drives the rapid lung scarring (pulmonary fibrosis) seen in severe COVID-19. The findings point to specific fibroblast proteins that may serve as drug targets to block deleterious effects.
Regev’s team also describes how the virus affects other parts of the body. One surprising discovery was there was scant evidence of direct SARS-CoV-2 infection in the liver, kidney, or heart tissue of the deceased. Yet, a closer look heart tissue revealed widespread damage, documenting that many different coronary cell types had altered their genetic programs. It’s still to be determined if that’s because the virus had already been cleared from the heart prior to death. Alternatively, the heart damage might not be caused directly by SARS-CoV-2, and may arise from secondary immune and/or metabolic disruptions.
Together, these two studies provide clearer pictures of the pathology in the most severe and lethal cases of COVID-19. The data from these cell atlases has been made freely available for other researchers around the world to explore and analyze. The hope is that these vast data sets, together with future analyses and studies of people who’ve tragically lost their lives to this pandemic, will improve our understanding of long-term complications in patients who’ve survived. They also will now serve as an important foundational resource for the development of promising therapies, with the goal of preventing future complications and deaths due to COVID-19.
 A molecular single-cell lung atlas of lethal COVID-19. Melms JC, Biermann J, Huang H, Wang Y, Nair A, Tagore S, Katsyv I, Rendeiro AF, Amin AD, Schapiro D, Frangieh CJ, Luoma AM, Filliol A, Fang Y, Ravichandran H, Clausi MG, Alba GA, Rogava M, Chen SW, Ho P, Montoro DT, Kornberg AE, Han AS, Bakhoum MF, Anandasabapathy N, Suárez-Fariñas M, Bakhoum SF, Bram Y, Borczuk A, Guo XV, Lefkowitch JH, Marboe C, Lagana SM, Del Portillo A, Zorn E, Markowitz GS, Schwabe RF, Schwartz RE, Elemento O, Saqi A, Hibshoosh H, Que J, Izar B. Nature. 2021 Apr 29.
 COVID-19 tissue atlases reveal SARS-CoV-2 pathology and cellular targets. Delorey TM, Ziegler CGK, Heimberg G, Normand R, Shalek AK, Villani AC, Rozenblatt-Rosen O, Regev A. et al. Nature. 2021 Apr 29.
COVID-19 Research (NIH)
Izar Lab (Columbia University, New York)
Aviv Regev (Genentech, South San Francisco, CA)
NIH Support: National Center for Advancing Translational Sciences; National Heart, Lung, and Blood Institute; National Cancer Institute; National Institute of Allergy and Infectious Diseases; National Institute of Diabetes and Digestive and Kidney Diseases; National Human Genome Research Institute; National Institute of Mental Health; National Institute on Alcohol Abuse and Alcoholism
Posted on by Dr. Francis Collins
It was an amazing experience to touch base once again with Kate Rubins, a NASA astronaut aboard the International Space Station. Connecting via live downlink on March 26, 2021, we discussed how space-based research can enable valuable biomedical advances on our planet. For example, over the past five years, NIH’s National Center for Advancing Translational Sciences has funded a series of tissue chip payloads that have launched to the orbiting laboratory. Rubins, who is a biologist and infectious disease expert, has facilitated three of these projects: Cardinal Heart from Stanford University, Electrical Stimulation of Human Myocytes in Microgravity from the University of Florida, and Cartilage-Bone-Synovium from the Massachusetts Institute of Technology.
Posted on by Dr. Francis Collins
There’s been quite a bit of discussion in the news lately about whether to pause or resume college athletics during the pandemic. One of the sticking points has been uncertainty about how to monitor the health of student athletes who test positive for SARS-CoV-2, the novel coronavirus that causes COVID-19. As a result, college medical staff don’t always know when to tell athletes that they’ve fully recovered and it’s safe to start training again.
The lack of evidence owes to two factors. Though it may not seem like it, this terrible coronavirus has been around for less than a year, and that’s provided little time to conduct the needed studies with young student athletes. But that’s starting to change. An interesting new study in the journal JAMA Cardiology provides valuable and rather worrisome early data from COVID-positive student athletes evaluated for an inflammation of the heart called myocarditis, a well-known complication .
Saurabh Rajpal and his colleagues at the Ohio State University, Columbus, used cardiac magnetic resonance imaging (MRI) to visualize the hearts of 26 male and female student athletes. They participated in a range of sports, including football, soccer, lacrosse, basketball, and track. All of the athletes were referred to the university’s sports medicine clinic this past summer after testing positive for SARS-CoV-2. All had mild or asymptomatic cases of COVID-19.
Even so, the MRI scans, taken 11-53 days after completion of quarantine, showed four of the student athletes (all males) had swelling and tissue damage to their hearts consistent with myocarditis. Although myocarditis often resolves on its own over time, severe cases can compromise the heart muscle’s ability to beat. That can lead to heart failure, abnormal heart rhythms, and even sudden death in competitive athletes with normal heart function .
The investigators also looked for more subtle findings of cardiac injury in these athletes, using a contrast agent called gadolinium and measuring its time to appear in the cardiac muscle during the study. Eight of the 26 athletes (31 percent) had late gadolinium enhancement, suggestive of prior myocardial injury.
Even though it’s a small study, these results certainly raise concerns. They add more evidence to a prior study, published by a German group, that suggested subtle cardiac consequences of SARS-CoV-2 infection may be common in adults .
Rajpal and his colleagues will continue to follow the athletes in their study for several more months. The researchers will keep an eye out for other lingering symptoms of COVID-19, generate more cardiac MRI data, and perform exercise testing.
As this study shows, we still have a lot to learn about the long-term consequences of COVID-19, which can take people on different paths to recovery. For athletes, that path is the challenge to return to top physical shape and feel ready to compete at a high level. But getting back in uniform must also be done safely to minimize any risks to an athlete’s long-term health and wellbeing. The more science-based evidence that’s available, the more prepared athletes at large and small colleges will be to compete safely in this challenging time.
 Cardiovascular magnetic resonance findings in competitive athletes recovering from COVID-19 infection. Rajpal S, Tong MS, Borchers J, et al. JAMA Cardiol. 2020 September 11. [Published online ahead of print.]
 Eligibility and disqualification recommendations for competitive athletes with cardiovascular abnormalities: Task Force 3: Hypertrophic cardiomyopathy, arrhythmogenic right ventricular cardiomyopathy and other cardiomyopathies, and myocarditis. Maron BJ, Udelson JE, Bonow RO, et al. Circulation. 2015;132(22):e273-e280.
 Outcomes of cardiovascular magnetic resonance imaging in patients recently recovered from Coronavirus Disease 2019 (COVID-19). Puntmann VO, Carej ML, Wieters I. JAMA Cardiol. 2020 Jul 27:e203557. [Published online ahead of print.]
Coronavirus (COVID-19) (NIH)
Heart Inflammation (National Heart, Lung, and Blood Institute/NIH)
Saurabh Rajpal (Ohio State College of Medicine, Columbus)
Posted on by Dr. Francis Collins
Most children infected with SARS-CoV-2, the virus that causes COVID-19, develop only a mild illness. But, days or weeks later, a small percentage of kids go on to develop a puzzling syndrome known as multisystem inflammatory syndrome in children (MIS-C). This severe inflammation of organs and tissues can affect the heart, lungs, kidneys, brain, skin, and eyes.
Thankfully, most kids with MIS-C respond to treatment and make rapid recoveries. But, tragically, MIS-C can sometimes be fatal.
With COVID-19 cases in children having increased by 21 percent in the United States since early August , NIH and others are continuing to work hard on getting a handle on this poorly understood complication. Many think that MIS-C isn’t a direct result of the virus, but seems more likely to be due to an intense autoimmune response. Indeed, a recent study in Nature Medicine  offers some of the first evidence that MIS-C is connected to specific changes in the immune system that, for reasons that remain mysterious, sometimes follow COVID-19.
These findings come from Shane Tibby, a researcher at Evelina London Children’s Hospital, London. United Kingdom; Manu Shankar-Hari, a scientist at Guy’s and St Thomas’ NHS Foundation Trust, London; and colleagues. The researchers enlisted 25 children, ages 7 to 14, who developed MIS-C in connection with COVID-19. In search of clues, they examined blood samples collected from the children during different stages of their care, starting when they were most ill through recovery and follow-up. They then compared the samples to those of healthy children of the same ages.
What they found was a complex array of immune disruptions. The children had increased levels of various inflammatory molecules known as cytokines, alongside raised levels of other markers suggesting tissue damage—such as troponin, which indicates heart muscle injury.
The neutrophils, monocytes, and other white blood cells that rapidly respond to infections were activated as expected. But the levels of certain white blood cells called T lymphocytes were paradoxically reduced. Interestingly, despite the low overall numbers of T lymphocytes, particular subsets of them appeared activated as though fighting an infection. While the children recovered, those differences gradually disappeared as the immune system returned to normal.
It has been noted that MIS-C bears some resemblance to an inflammatory condition known as Kawasaki disease, which also primarily affects children. While there are similarities, this new work shows that MIS-C is a distinct illness associated with COVID-19. In fact, only two children in the study met the full criteria for Kawasaki disease based on the clinical features and symptoms of their illness.
Another recent study from the United Kingdom, reported several new symptoms of MIS-C . They include headaches, tiredness, muscle aches, and sore throat. Researchers also determined that the number of platelets was much lower in the blood of children with MIS-C than in those without the condition. They proposed that evaluating a child’s symptoms along with his or her platelet level could help to diagnose MIS-C.
It will now be important to learn much more about the precise mechanisms underlying these observed changes in the immune system and how best to treat or prevent them. In support of this effort, NIH recently announced $20 million in research funding dedicated to the development of approaches that identify children at high risk for developing MIS-C .
The hope is that this new NIH effort, along with other continued efforts around the world, will elucidate the factors influencing the likelihood that a child with COVID-19 will develop MIS-C. Such insights are essential to allow doctors to intervene as early as possible and improve outcomes for this potentially serious condition.
 Peripheral immunophenotypes in children with multisystem inflammatory syndrome associated with SARS-CoV-2 infection. Carter MJ, Fish M, Jennings A, Doores KJ, Wellman P, Seow J, Acors S, Graham C, Timms E, Kenny J, Neil S, Malim MH, Tibby SM, Shankar-Hari M. Nat Med. 2020 Aug 18.
 Children and COVID-19: State-Level Data Report. American Academy of Pediatrics. August 24, 2020.
 Clinical characteristics of children and young people admitted to hospital with covid-19 in United Kingdom: prospective multicentre observational cohort study. Swann OV, Holden KA, Turtle L, Harrison EW, Docherty AB, Semple MG, et al. Br Med J. 2020 Aug 17.
 NIH-funded project seeks to identify children at risk for MIS-C. NIH. August 7, 2020.
Coronavirus (COVID-19) (NIH)
Kawasaki Disease (Genetic and Rare Disease Information Center/National Center for Advancing Translational Sciences/NIH)
Shane Tibby (Evelina London Children’s Hospital, London)
Manu Shankar-Hari (King’s College, London)
NIH Support: Eunice Kennedy Shriver National Institute of Child Health and Human Development; Office of the Director; National Heart, Lung, and Blood Institute; National Institute of Allergy and Infectious Diseases; National Institute of Arthritis and Musculoskeletal and Skin Diseases; National Institute on Drug Abuse; National Institute of Minority Health and Health Disparities; Fogarty International Center
Posted on by Dr. Francis Collins
Watch this brief video and you might guess you’re seeing an animated line drawing, gradually revealing a delicate take on a familiar system: the internal structures of the human body. But this movie doesn’t capture the work of a talented sketch artist. It was created using the first 3D, full-body imaging device using positron emission tomography (PET).
The device is called an EXPLORER (EXtreme Performance LOng axial REsearch scanneR) total-body PET scanner. By pairing this scanner with an advanced method for reconstructing images from vast quantities of data, the researchers can make movies.
For this movie in particular, the researchers injected small amounts of a short-lived radioactive tracer—an essential component of all PET scans—into the lower leg of a study volunteer. They then sat back as the scanner captured images of the tracer moving up the leg and into the body, where it enters the heart. The tracer moves through the heart’s right ventricle to the lungs, back through the left ventricle, and up to the brain. Keep watching, and, near the 30-second mark, you will see in closer focus a haunting capture of the beating heart.
This groundbreaking scanner was developed and tested by Jinyi Qi, Simon Cherry, Ramsey Badawi, and their colleagues at the University of California, Davis . As the NIH-funded researchers reported recently in Proceedings of the National Academy of Sciences, their new scanner can capture dynamic changes in the body that take place in a tenth of a second . That’s faster than the blink of an eye!
This movie is composed of frames captured at 0.1-second intervals. It highlights a feature that makes this scanner so unique: its ability to visualize the whole body at once. Other medical imaging methods, including MRI, CT, and traditional PET scans, can be used to capture beautiful images of the heart or the brain, for example. But they can’t show what’s happening in the heart and brain at the same time.
The ability to capture the dynamics of radioactive tracers in multiple organs at once opens a new window into human biology. For example, the EXPLORER system makes it possible to measure inflammation that occurs in many parts of the body after a heart attack, as well as to study interactions between the brain and gut in Parkinson’s disease and other disorders.
EXPLORER also offers other advantages. It’s extra sensitive, which enables it to capture images other scanners would miss—and with a lower dose of radiation. It’s also much faster than a regular PET scanner, making it especially useful for imaging wiggly kids. And it expands the realm of research possibilities for PET imaging studies. For instance, researchers might repeatedly image a person with arthritis over time to observe changes that may be related to treatments or exercise.
Currently, the UC Davis team is working with colleagues at the University of California, San Francisco to use EXPLORER to enhance our understanding of HIV infection. Their preliminary findings show that the scanner makes it easier to capture where the human immunodeficiency virus (HIV), the cause of AIDS, is lurking in the body by picking up on signals too weak to be seen on traditional PET scans.
While the research potential for this scanner is clearly vast, it also holds promise for clinical use. In fact, a commercial version of the scanner, called uEXPLORER, has been approved by the FDA and is in use at UC Davis . The researchers have found that its improved sensitivity makes it much easier to detect cancers in patients who are obese and, therefore, harder to image well using traditional PET scanners.
As soon as the COVID-19 outbreak subsides enough to allow clinical research to resume, the researchers say they’ll begin recruiting patients with cancer into a clinical study designed to compare traditional PET and EXPLORER scans directly.
As these researchers, and other researchers around the world, begin to put this new scanner to use, we can look forward to seeing many more remarkable movies like this one. Imagine what they will reveal!
 First human imaging studies with the EXPLORER total-body PET scanner. Badawi RD, Shi H, Hu P, Chen S, Xu T, Price PM, Ding Y, Spencer BA, Nardo L, Liu W, Bao J, Jones T, Li H, Cherry SR. J Nucl Med. 2019 Mar;60(3):299-303.
 Subsecond total-body imaging using ultrasensitive positron emission tomography. Zhang X, Cherry SR, Xie Z, Shi H, Badawi RD, Qi J. Proc Natl Acad Sci U S A. 2020 Feb 4;117(5):2265-2267.
 “United Imaging Healthcare uEXPLORER Total-body Scanner Cleared by FDA, Available in U.S. Early 2019.” Cision PR Newswire. January 22, 2019.
Positron Emission Tomography (PET) (NIH Clinical Center)
EXPLORER Total-Body PET Scanner (University of California, Davis)
Cherry Lab (UC Davis)
Badawi Lab (UC Davis Medical Center, Sacramento)
NIH Support: National Cancer Institute; National Institute of Biomedical Imaging and Bioengineering; Common Fund
Posted on by Dr. Francis Collins
It is now possible to pull up the design of a guitar on a computer screen and print out its parts on a 3D printer equipped with special metal or plastic “inks.” The same technological ingenuity is also now being applied with bioinks—printable gels containing supportive biomaterials and/or cells—to print out tissue, bone, blood vessels, and, even perhaps one day, viable organs.
While there’s a long way to go until then, a team of researchers has reached an important milestone in bioprinting collagen and other extracellular matrix proteins that undergird every tissue and organ in the body. The researchers have become so adept at it that they now can print biomaterials that mimic the structural, mechanical, and biological properties of real human tissues.
Take a look at the video. It shows a life-size human heart valve that’s been printed with their improved collagen bioink. As fluid passes through the aortic valve in a lab test, its three leaf-like flaps open and close like the real thing. All the while, the soft, flexible valve withstands the intense fluid pressure, which mimics that of blood flowing in and out of a beating heart.
The researchers, led by NIH grantee Adam Feinberg, Carnegie Mellon University, Pittsburgh, PA, did it with their latest version of a 3D bioprinting technique featured on the blog a few years ago. It’s called: Freeform Reversible Embedding of Suspended Hydrogels v.2.0. Or, just FRESH v2.0.
The FRESH system uses a bioink that consists of collagen (or other soft biomaterials) embedded in a thick slurry of gelatin microparticles and water. While a number of technical improvements have been made to FRESH v. 2.0, the big one was getting better at bioprinting collagen.
The secret is to dissolve the collagen bioink in an acid solution. When extruded into a neutral support bath, the change in pH drives the rapid assembly of collagen. The ability to extrude miniscule amounts and move the needle anywhere in 3D space enables them to produce amazingly complex, high-resolution structures, layer by layer. The porous microstructure of the printed collagen also helps for incorporating human cells. When printing is complete, the support bath easily melts away by heating to body temperature.
As described in Science, in addition to the working heart valve, the researchers have printed a small model of a heart ventricle. By combining collagen with cardiac muscle cells, they found they could actually control the organization of muscle tissue within the model heart chamber. The 3D-printed ventricles also showed synchronized muscle contractions, just like you’d expect in a living, beating human heart!
That’s not all. Using MRI images of an adult human heart as a template, the researchers created a complete organ structure including internal valves, large veins, and arteries. Based on the vessels they could see in the MRI, they printed even tinier microvessels and showed that the structure could support blood-like fluid flow.
While the researchers have focused the potential of FRESH v.2.0 printing on a human heart, in principle the technology could be used for many other organ systems. But there are still many challenges to overcome. A major one is the need to generate and incorporate billions of human cells, as would be needed to produce a transplantable human heart or other organ.
Feinberg reports more immediate applications of the technology on the horizon, however. His team is working to apply FRESH v.2.0 for producing child-sized replacement tracheas and precisely printed scaffolds for healing wounded muscle tissue.
Meanwhile, the Feinberg lab generously shares its designs with the scientific community via the NIH 3D Print Exchange. This innovative program is helping to bring more 3D scientific models online and advance the field of bioprinting. So we can expect to read about many more exciting milestones like this one from the Feinberg lab.
 3D bioprinting of collagen to rebuild components of the human heart. Lee A, Hudson AR, Shiwarski DJ, Tashman JW, Hinton TJ, Yerneni S, Bliley JM, Campbell PG, Feinberg AW. Science. 2019 Aug 2;365(6452):482-487.
Tissue Engineering and Regenerative Medicine (National Institute of Biomedical Imaging and Bioengineering/NIH)
Regenerative Biomaterials and Therapeutics Group (Carnegie Mellon University, Pittsburgh, PA)
FluidForm (Acton, MA)
3D Bioprinting Open Source Workshops (Carnegie Mellon)
Video: Adam Feinberg on Tissue Engineering to Treat Human Disease (YouTube)
NIH Support: National Heart, Lung, and Blood Institute; Eunice Kennedy Shriver National Institute of Child Health and Human Development; Common Fund