Publisher Health

A new study reported that SARS-CoV-2, the virus that causes COVID, can infect dopamine neurons in the brain and trigger senescence — when a cell loses the ability to grow and divide. The researchers from Weill Cornell Medicine, Memorial Sloan Kettering Cancer Center and Columbia University Vagelos College of Physicians and Surgeons suggest that further research on this finding may shed light on the neurological symptoms associated with long COVID such as brain fog, lethargy and depression.
The findings, published in Cell Stem Cell on Jan. 17, show that dopamine neurons infected with SARS-CoV-2 stop working and send out chemical signals that cause inflammation. Normally, these neurons produce dopamine, a neurotransmitter that plays a role in feelings of pleasure, motivation, memory, sleep and movement. Damage to these neurons is also connected to Parkinson’s disease.
“This project started out to investigate how various types of cells in different organs respond to SARS-CoV-2 infection. We tested lung cells, heart cells, pancreatic beta cells, but the senescence pathway is only activated in dopamine neurons,” said senior author Dr. Shuibing Chen, director of the Center for Genomic Health, the Kilts Family Professor Surgery and a member of the Hartman Institute for Therapeutic Organ Regeneration at Weill Cornell Medicine. “This was a completely unexpected result.”
Determining How SARS-CoV-2 Impacts Different Cells
Previously, Dr. Chen led the effort to generate multiple cell types from human stem cells and tested them to see which ones SARS-CoV-2 could infect. This allowed the researchers to survey the spectrum of tissues that might be infected during COVID, which has a diverse array of symptoms in different patients. They also studied autopsy samples from patients infected with the virus to confirm their observations from the lab grown cells.
Surprisingly, they found that a small percentage of dopamine neurons exposed to SARS-CoV-2 were infected, approximately five percent. “The infection rate of dopamine neurons isn’t as high as lung cells, the virus’s main target, but even a small population of infected cells can potentially have a severe effect,” said Dr. Chen.
Interestingly, not all neuronal cell types were vulnerable to viral infection. The researchers observed that cortical neurons were not permissive to SARS-CoV-2 infection under identical experimental conditions.

Protecting Dopamine Neurons
In this paper, the researchers used transcriptional profiling to identify how SARS-CoV-2 infection modified gene activity and the resulting changes in the way cells behaved. “We discovered that only dopamine cells had the senescence pathway activated,” said Dr. Chen. In stark contrast, the genes in the senescence pathway were not significantly turned on with SARS-CoV-2 infected lung organoids, pancreatic cells, liver organoids or heart cells.
The researchers found that the gene signatures — the unique pattern of gene activity — from the infected lab-grown dopamine neurons and the dopamine neurons from COVID autopsy samples were the same. This included genes that triggered chemical signals for inflammation.
Next, they looked for ways to protect the neurons to reduce the risk of neurological defects when a patient is infected by the virus.
The researchers tested drugs already marketed for various conditions to find one that either prevented SARS-CoV-2 infection or rescued infected dopamine neurons from senescence. The screen identified three drugs that blocked SARS-CoV-2 infection thereby preventing the dopamine cells from senescence: riluzole (treats ALS or Lou Gehrig’s disease), metformin (treats diabetes) and imatinib (treats cancer). Further study on these drugs may lead to a way to prevent the virus’s attack on the brain.
Though most people are exposed to COVID, only certain individuals will be impacted since many factors are involved in the risk for neurological symptoms including severity of the disease and genetics. Human population studies are exploring this aspect further.
While the clinical relevance of these findings is still unclear, since dopamine neuron senescence is a hallmark of Parkinson’s disease the researchers suggest that long COVID patients should be monitored for an increased risk of developing Parkinson’s-related symptoms. To date Parkinson’s symptoms have not been overly reported in population studies.
This study was a collaboration with Dr. Lorenz Studer, director of the Center for Stem Cell Biology at Memorial Sloan Kettering Cancer Center; Dr. David D. Ho, Clyde ’56 and Helen Wu Professor of Medicine at Columbia University Vagelos College of Physicians and Surgeons; and Dr. Robert Schwartz, associate professor of medicine in the Division of Gastroenterology and Hepatology, a member of the Sandra and Edward Meyer Cancer Center at Weill Cornell Medicine and a hepatologist at NewYork-Presbyterian/Weill Cornell Medical Center.

Deaths from breast cancer dropped 58% between 1975 and 2019 due to a combination of screening mammography and improvements in treatment, according to a new multicenter study led by Stanford Medicine clinicians and biomedical data scientists.
Nearly one-third of the decrease (29%) is due to advances in treating metastatic breast cancer — a form that has spread to other areas of in the body and is known as stage 4 breast cancer or recurrent cancer. Although these advanced cancers are not considered curable, women with metastatic disease are living longer than ever.
The analysis helps cancer researchers assess where to focus future efforts and resources.
“We’ve known that deaths from breast cancer have been decreasing over the past several decades, but it’s been difficult or impossible to quantify which of our interventions have been most successful, and to what extent,” said Jennifer Caswell-Jin, MD, assistant professor of medicine. “This type of study allows us to see which of our efforts are having the most impact and where we still need to improve.”
Caswell-Jin and Liyang Sun are co-first authors of the study, which was published Jan. 16 in the Journal of the American Medical Association. Sylvia Plevritis, PhD, professor and chair of biomedical data science, and Allison Kurian, MD, MSc, professor of medicine and of epidemiology and population health, are co-senior authors.
The study was a collaborative effort by a national consortium of researchers called CISNET, or the Cancer Intervention and Surveillance Modeling Network. CISNET was established in 2000 by the National Cancer Institute to understand the impact of cancer surveillance, screening and treatment on incidence and mortality. Doing so requires sophisticated computer algorithms capable of modeling the natural course of the disease and the typical treatment paths of individual patients, then translating that information to population-level data collected by the national Surveillance, Epidemiology, and End Results Program, or SEER registry, from 1975 to 2019.
The study is the third in a trio of papers from CISNET published since 2005 that assess the relative contributions of regular screening and treatment advances on breast cancer deaths. The previous two papers informed national guidelines and helped cancer researchers focus their efforts on the most intractable problems.

“Twenty years ago, there was a question whether routine screening mammography actually decreased the number of deaths from breast cancer,” Plevritis said. But in 2005, she and other CISNET researchers published a paper in the New England Journal of Medicine that conclusively demonstrated that screening was responsible for anywhere from 28% to 65% (different models came up with varying degrees of impact) of the reduction in mortality by 2000 between 1975 and 2000.
The second paper, published in 2018 in the Journal of the American Medical Association, highlighted the differences in treatment responsiveness and survival outcomes among women with differing breast cancer subtypes from 2000 to 2012 — pinpointing subgroups with poorer survival.
“We found that, while screening still had an important impact, most of the decline in annual deaths was due to improvements in treating early-stage breast cancer based on each cancer’s molecular profile,” Plevritis said.
The current study is the first to explicitly include patients with metastatic breast cancer in its models. The finding that 29% of the decrease in mortality is due to advances in treating metastatic breast cancer both surprised and gratified the researchers.
“Initially, we assumed that treatment of advanced disease was unlikely to make a significant contribution to the declines in mortality we documented in the previous two papers,” Caswell-Jin said. “But our treatments have improved, and it’s clear that they are having a significant impact on annual mortality.”
The CISNET researchers used four computer models to assess the SEER data from 1975 to 2019 — one developed at Stanford Medicine in the Plevritis Lab, one by researchers at the Dana-Farber Cancer Institute, one at MD Anderson Cancer Center, and another jointly developed by researchers at the University of Wisconsin and Harvard Medical School. The four models came up with remarkably similar estimates for the impact of each intervention: screening mammography, treatment of early-stage (stages 1, 2 or 3) breast cancer and treatment of metastatic breast cancer.

The models reproduced the decline in mortality in breast cancer known from SEER data, from 48 per 100,000 women dying of breast cancer each year in 1975 to 27 per 100,000 in 2019 — a decrease of about 44%. The models arrived at a larger estimated reduction in mortality of about 58% because the incidence of breast cancer has risen during the same period and more women would have died had screening and treatments not improved.
The models concluded that about 47% of this reduction in mortality is the result of improved treatments for early-stage breast cancer, and about 25% is attributed to screening mammography. The remainder, or about 29%, is due to improvements in treating metastatic disease.
“Designing the new model, which had to account for individuals with non-metastatic cancer who underwent treatment but later progressed to metastatic cancer, and who may have been treated with multiple drugs over the course of their disease, was extremely complex,” Plevritis said. “It took about four years. But it was really satisfying when we were able to validate the model’s behavior and see that all four models from different institutions, which used the new model inputs in different ways, delivered consistent findings. The models not only make sense, but also produce meaningful insights.”
The impact of treating metastatic disease is exemplified by the increases in median survival time after metastasis: Patients diagnosed in 2000 with metastatic disease lived an average of 1.9 years versus an average of 3.2 years for those diagnosed in 2019. Survival time varies by subgroup status, however. Patients with what are known as estrogen receptor-positive and HER2 positive cancers saw an average increase in survival time of 2.5 years. Those with estrogen receptor-positive and HER2-negative cancers lived an average of 1.6 years longer, but those with cancers that are estrogen receptor-negative and HER2-negative lived about 0.5 years longer in 2019 than in 2000.
“It was meaningful as a breast oncologist to spend time with this history and see real progress over the past decades,” Caswell-Jin said. “There is much more work to be done; metastatic breast cancer isn’t yet curable. But it is rewarding to see that advances have made a difference in these numbers,” she added. “Our scientific and clinical work is helping our patients live longer, and I believe deaths from breast cancer will continue to steadily decline as innovation continues to grow.”
Researchers from MD Anderson Cancer Center, the Dana-Farber Cancer Institute, the University of Wisconsin-Madison School of Medicine and Public Health, the National Institutes of Health, the Albert Einstein College of Medicine, Harvard Medical School, Georgetown University, and the Georgetown-Lombardi Institute for Cancer and Aging contributed to the study.
The study was funded by the National Institutes of Health (grants U01CA253911 and U01CA199218).

The blueprint for human life lies within the DNA in the nucleus of each of our cells. In human cells, around six and a half feet of this genetic material must be condensed to fit inside the nucleus. DNA condensation is not random. To function properly, the genetic material is highly organized into loop structures that often bring together widely separated sections of the genome critical to the regulation of gene activity. In a new paper published in Nature Communications, USC Stem Cell scientists from the laboratory of Oliver Bell address how these loops can help repress or silence gene activity, with potentially far-reaching effects on human health.
“A carefully orchestrated regulatory machinery is required to ensure every cell in the body is expressing its correct gene set to exert its dedicated function,” said the study’s first author Daniel Bsteh, who began the research at the Institute of Molecular Biotechnology of the Austrian Academy of Sciences (IMBA), and completed it at the Keck School of Medicine of USC during his PhD. He is currently the Liquid Biopsy Core Manager at the USC Norris Comprehensive Cancer Center.
In the study, Bsteh and his colleagues specifically examined developmental genes that are repressed by molecules known as Polycomb Repressive Complexes 1 and 2 (PRC1 and PRC2). PRC1 and PRC2 are regulators that prevent developmental genes from becoming activated at the wrong time or in the wrong cell, which has been shown to cause changes in cellular identity, leading to developmental defects, or transformation into cancer cells.
When PRC1- and PRC2-repressed genes come together, the genome forms loops. Loops are known to play a role in activating genes, but it has been more challenging to study how loops might help repress genes. This is because of the interdependence of loops with a different type of gene repressing mechanism known as histone modifications.
Through a genetic screen conducted in mouse embryonic stem cells, the scientists identified a protein, PDS5A, that modifies loops without affecting histone modifications. This enabled Bsteh and colleagues to specifically study the effects of loops and 3D genome organization on gene silencing.
The loss of PDS5A disrupted the loops — and therefore the long-range interactions between repressed developmental genes. Further, looping genes together maintains the silent state. When PRC1- and PRC2-repressed genes are physically separated, eliminating the loops, normally silent genes become activated in aberrant ways.
“PDS5A is a subunit of a larger protein complex called cohesin, which is the master regulator of 3D genome organization,” said Bell, an assistant professor of biochemistry and molecular medicine, and stem cell biology and regenerative medicine, and a member of the USC Norris Comprehensive Cancer Center. “Cohesin mutations are known to drive several human diseases, including developmental disorders and cancer. What’s striking about our discovery is that it reveals a dependence of PRC 1 and PRC 2 activity on the precise regulation of 3D genome organization by cohesin, suggesting that ‘cohesinopathies’ may be linked to aberrant developmental gene silencing.”
Additional authors include Hagar F. Moussa, Georg Michlits, Ramesh Yelagandula, Jingkui Wang, and Ulrich Elling from the IMBA.
Support for this research came from the Austrian Academy of Sciences, the New Frontiers Group of the Austrian Academy of Sciences (grant NFG-05), the Human Frontiers Science Program Career Development Award (CDA00036/2014-C), and startup funding from the USC Norris Comprehensive Cancer Center.

A spider venom molecule being investigated by a University of Queensland team has met critical benchmarks towards becoming a treatment for heart attack and stroke.
Associate Professor Nathan Palpant and Professor Glenn King from UQ’s Institute for Molecular Bioscience have previously shown that the drug candidate Hi1a protectscells from the damage caused by heart attack and stroke.
Dr Palpant said a subsequent study has put the drug through a series of preclinical tests designed to mimic real-life treatment scenarios.
“These tests are a major step towards helping us understand how Hi1a would work as a therapeutic — at what stage of a heart attack it could be used and what the doses should be,” Dr Palpant said.
“We established that Hi1a is as effective at protecting the heart as the only cardioprotective drug to reach Phase 3 clinical trials, a drug that was ultimately shelved due to side effects.
“Importantly, we found that Hi1a only interacts with cells in the injured zone of the heart during an attack and doesn’t bind to healthy regions of the heart — reducing the chance of side effects.”
Professor King, who recently won the Prime Minister’s Prize for Innovation for developing the world’s first insecticides from spider venom, discovered Hi1a in the venom of the K’gari funnel web spider.

“Hi1a could reduce damage to the heart and brain during heart attacks and strokes by preventing cell death caused by lack of oxygen,” Professor King said.
“Our testing and safety studies from independent contract research organisations has provided evidence that Hi1a could be an effective and safe therapeutic.”
Infensa Bioscience, a company co-founded by the researchers, raised $23 million in 2022 to develop Hi1a for commercial purposes.
Infensa CEO and UQ researcher, Associate Professor Mark Smythe, said cardiovascular disease is the leading cause of death globally.
“Most deaths from cardiovascular disease are caused by heart attacks and strokes, yet there are no drugs on the market that prevent the damage they cause,” Dr Smythe said.
“An effective drug to treat heart attacks would have worldwide impact, providing a breakthrough to improve the lives of millions of individuals living with heart disease.”
The research team included Dr Meredith Redd from IMB as well as Dr Melissa Reichelt and Dr Yusuke Yoshikawa from UQ’s School of Biomedical Sciences.

A team of South Korean scientists led by Professor KIM Jae Kyoung of the Biomedical Mathematics Group within the Institute for Basic Science (IBS-BIMAG) discovered the secrets of cell variability in our bodies. The findings of this research are expected to have far-reaching effects, such as improvement in the efficacy of chemotherapy treatments, or set a new paradigm in the study of antibiotic-resistant bacteria.
The cells in our body have a signaling system that responds to various external stimuli such as antibiotics and osmotic pressure changes. This signaling system plays a critical role in the survival of cells as they interact with the external environment. However, even cells with same genetic information can respond differently to the same external stimuli, called cellular heterogeneity.
Cellular heterogeneity is a great research interest in medicine, as it is known to hinder the complete eradication of cancer cells by chemotherapeutic agents such as anticancer drugs. The sources of such heterogeneity and its relationship with the signaling system have remained a challenge, as intermediate processes of the signaling system are impossible to fully observe with current experimental technology.
To reveal the sources of this heterogeneity, Professor Kim’s research team developed a machine learning methodology using artificial neural network structures called Density Physics-informed neural networks (Density-PINNs). Density-PINNs use the observable time-series data of cells’ responses to external stimuli to inversely estimate information about the signaling system. By applying Density-PINNs to actual experimental data of antibiotic responses of bacterial cells (Escherichia coli), the research team found that a parallel structure of the signaling system can reduce heterogeneity among cells.
Professor Kim believes that this mathematical modeling and machine learning research will facilitate the enhancement of the understanding of cellular heterogeneity, which is crucial in cancer treatment. He expressed his hope that this achievement would lead to the development of improved cancer treatment strategies.
Dr. JO Hyeontae and Dr. HONG Hyukpyo participated as co-first authors in this research, which was published in the international journal Patterns (Impact Factor 6.5), a sister journal of Cell. The title of the paper is “Density Physics-informed Neural Networks Reveal Sources of Cell Heterogeneity in Signal Transduction.”

Cytokines are chemical messengers that help the body get rid of invading bacteria and viruses, and control inflammation. The body carefully balances cytokines because they help keep the immune system healthy. However, this balance is upset if the immune system overreacts. A serious infection or a severe burn can unleash a cytokine storm in the body. During the storm — also called cytokine release syndrome (CRS) — the body produces too many cytokines, leading to life-threatening inflammation.
Interleukin-6 (IL-6) is a key cytokine in the storm because it helps to drive the inflammation that damages the body. IL-6 delivers its message by fastening to IL-6 receptors within cells, which tells the cells to spread inflammation. Because IL-6 is important in CRS, treatments that block the IL-6 signal can relieve inflammation. However, this blocking tends to be long-lasting, which leads to side effects.
In a study published this month in the Proceedings of the National Academy of Sciences (PNAS), researchers from Osaka University have discovered a way to block IL-6 signals while minimizing treatment side effects. The group interrupted the inflammatory signal using an antibody that blocks the IL-6 receptor for only a short time. The brief interruption was long enough to protect the tissues against injury from cytokine storms caused by sepsis or severe burns.
“Our results suggest that CRS can be treated with an IL-6 receptor antibody that has a short half-life,” says the study’s lead author Sujin Kang. “This can prevent vascular damage and at the same time reduce the side effects associated with blocking IL-6.”
Vascular damage happens when an infection or burn causes the cells that line the inner surface of blood vessels to become leaky. The leaking fluid triggers a cytokine storm and can cause a secondary infection. The group also reported a potential mechanism for this damage to cells. When IL-6 binds to its receptor it activates a protein called hypoxia-inducible factor-1α (HIF1α), which amplifies inflammation.
“We found that blocking the IL-6R-HIF1α signal strengthened vascular endothelial cells and improved vessel integrity. This helped to prevent leakage from the vessels and relieved the inflammation caused by CRS,” explains senior author Tadamitsu Kishimoto. “We hope this will help patients suffering from CRS and other inflammatory diseases in the future.”
Other diseases that can cause CRS include sepsis and acute respiratory distress syndrome, COVID-19 infection, and ischemia. People with traumatic injuries and those taking some cancer immunotherapies can also experience a cytokine storm. The findings of this study can hopefully provide an alternative therapeutic approach to patients with these conditions.

A study by researchers from Nanyang Technological University, Singapore (NTU Singapore) found that older adults who exercise with their spouse achieve lower physical activity levels than older adults without their spouse.
In a study of 240 participants in Singapore aged 54 to 72 years old, the NTU Singapore researchers from the Wee Kim Wee School of Communication and Information (WKWSCI) also found that those who received personalised feedback on their fitness trackers were more active than those who did not.
With many societies facing an ageing population, promoting healthy ageing, such as through physical activity, has become increasingly important. Findings from the NTU study suggest that it may be more effective to do so by encouraging older adults to exercise individually, said the researchers.
Dr Sapphire Lin, who led the research as a PhD student at NTU WKWSCI, said: “The average participant in our study is 60 years old and has been married to and living with the same spouse for 30 years. This suggests that the study participants have well-established routines that do not necessarily include exercising with their spouse. For these couples, changing daily habits could require a major reshuffling of set habits and routines ingrained in their family life after years of marriage. This makes incorporating exercise difficult and could lead to a demotivating effect.
Now a Research Fellow at the Centre for Population Health Research and Implementation, SingHealth, Dr Lin added: “Our research suggests that older adults looking to introduce exercise into their lifestyles may find it more effective to focus on changing their own routines rather than attempting to exercise as a couple and seeking to impose changes on their partner.”
The study was published in the International Journal of Human-Computer Interaction in October 2023. Also on the research team are Associate Professor Sonny Rosenthal from WKWSCI and Professor Rich Ling, who has retired from NTU.
Its exploration of active ageing aligns with the University’s research focus on health and society as part of its NTU 2025 five-year strategic plan.

How the study was conducted
To investigate the effects of exercising with one’s spouse and receiving real-time fitness feedback on the level of physical activity in older adults, the NTU researchers gave 240 participants a fitness tracker, which records information such as the number of steps taken, heart rate, distance covered, calories burned, minutes of activity, and sleep data.
The participants recruited were all married and living with their spouses and were aged between 54 and 72. They were subsequently divided into four groups: two groups of 30 couples each who would exercise as couples, and two groups of 60 individuals each who would exercise without their spouse. Half of these participants (30 couples and 60 individuals) received real-time fitness feedback from their fitness trackers, while the other half had their trackers’ real-time feedback disabled.
They collected data over 12 weeks on how consistently the participants met daily step thresholds of 5,000, 7,500, 10,000, and 15,000 steps, as well as their daily mean and median number of steps.
Lower daily step count for older couples who exercised together
Previous intervention studies found positive activity level effects for older adults exercising with a peer or buddy.

By contrast, this study found that the participants who took part in the study as a couple had lower mean and median step counts. They also met the high daily step counts of 7,500, 10,000 and 15,000 less frequently than those who participated individually without their spouses. The researchers believe that higher levels of physical activity would require a greater change in couples’ lifestyles, thereby making it harder to achieve.
These findings suggest that it may be more effective to encourage behavioural or lifestyle changes such as physical activity in older adults individually rather than in couples.
Real-time feedback helpful in achieving moderate levels of physical activity
The findings show that participants who received real-time feedback on their fitness trackers achieved daily step counts of 7,500 and 10,000 more frequently than those who did not receive real-time feedback, indicating that personalised feedback from fitness trackers positively affects older adults’ physical activity.
This is because feedback highlights the discrepancies between people’s current and desired state of physical activity, said the researchers. They added that receiving feedback that they have hit their targets also allows them to believe in their ability to reach the goal, which results in continued motivation towards a physically active lifestyle.
However, real-time feedback did not increase the frequency of older adults achieving low step counts of 5,000 steps or high step counts of 15,000. Researchers attribute this finding to the former being too easy for older adults to achieve and the latter too difficult. Older adults are more inclined to attain moderate step counts of 7,500 and 10,000, which are both challenging and engaging enough.
The research team is now exploring more in-depth analysis of the data collected from this study to inform policies that will encourage active ageing in seniors.
They are also looking into using this study model on older adults of lower socioeconomic status to explore how policies can narrow the gaps in health and technology inequalities and ensure that this population segment does not get left behind.

Due to the substantial clinical demand for artificial small-diameter vessels (SDVs), numerous commercial products have emerged. However, the majority of existing artificial SDVs lack an endothelial layer, leading to thrombosis. Fabricating artificial SDVs with a consistently uniform endothelial layer and adequate mechanical properties has proven exceptionally challenging.
Recently, a team of researchers — led by Professor Jinah Jang from the Department of Mechanical Engineering, the Department of Convergence IT Engineering, the Department of Life Sciences, and the School of Convergence Science and Technology and Research Professor Hyoryung Nam from the Department of Convergence IT Engineering at Pohang University of Science and Technology (POSTECH), and Professor Seung-Jae Lee from the Department of Mechanical Engineering and Dr. Hun-Jin Jeong from the Department of Mechanical Engineering at Wonkwang University — collaborated to address this issue. They recently employed cutting-edge 3D printing technology with a dragging technique to produce SDVs featuring pores capable of forming an endothelium. The findings of their research were published in the international journal Bioactive Materials.
The team innovated a dragging 3D printing technique enabling the fabrication of pore structures without the need for extra materials or devices while maintaining precise control over pore size. Employing this technique, they produced artificial SDVs with a porous, multilayered design. These vessels were then infused with a combination of human umbilical vein endothelial cells (HUVECs) and human aortic smooth muscle cells (HAoSMCs) using a natural polymeric bio-ink. Remarkably, the HUVECs migrated through the pores, reaching the innermost layer of the artificial SDV and establishing an endothelium with the extent of coverage dependent on the pore size.
The team achieved a coverage of up to 97.68 ± 0.4% of the artificial SDV surface with the endothelium, preventing platelet adhesion. This approach allowed the creation of an artificial SDV capable of autonomously forming its own endothelium solely through the presence of pores, eliminating the need for additional processing steps.
Professor Jinah Jang explained, “This research marks the first use of advanced dragging 3D printing technology and harnesses the properties of HUVECs for the development of spontaneous cellular assembly small diameter vessels (S-SDVs).” She added, “Their robust stability and mechanical characteristics not only render them suitable for transplantation but also position them as valuable for the future endothelialization of intricate vascular structures such as those with branches and curves.”
This study was conducted with the support from the Regenerative Medicine Project of the Ministry of Science and ICT, the National Research Foundation of Korea, and the Ministry of Health and Welfare, and the Korea Health Technology R&D Project of the Korea Health Industry Development Institute, and the Ministry of Trade, Industry & Energy.

Recently, high-speed video content capturing fleeting moments, such as bullets passing through glass, has captured people’s interest. What if we implement ultrasound used in medical examinations into high-speed video? A research team at POSTECH (Pohang University of Science and Technology) has solved the mystery of kidney diseases using ultrafast ultrasound that captures 1,000 images in just one second.
The research team led by Professor Chulhong Kim from the Department of Electrical Engineering, the Department of Convergence IT Engineering, the Department of Mechanical Engineering, and the School of Convergence Science and Technology, Professor Jinah Jang from the Department of Mechanical Engineering and the Department of Convergence IT Engineering, Professor Yong Joo Ahn from the Department of Convergence IT Engineering and the School of Convergence Science and Technology, Donghyeon Oh and Donghyun Lee, PhD candidates from the Department of Convergence IT Engineering, Jinseok Heo, a PhD candidate from the Department of Electrical Engineering, Jooyoung Kweon, a master’s student from the School of Convergence Science and Technology, and Uijung Yong, a postdoctoral researcher from the Future IT Innovation Laboratory at POSTECH has achieved imaging of the three-dimensional microvasculature of the kidneys using ultrafast ultrasound. Their technique is gathering attention, being capable of visualizing the whole kidney microvasculature without any contrast agents. The findings will be published as an inside back cover article in the international journal Advanced Science.
The kidney plays a role in filtering waste and eliminating unwanted substances from the bloodstream. Conditions such as hypertension and diabetes can compromise this vital function, leading to a kidney failure — irreversible condition necessitating lifelong treatment through artificial hemodialysis or donor kidney transplantation. Given the direct connection between blood perfusion in the kidneys and their filtration function, microvascular imaging can be a key indicator for both preventing and recovering from kidney failure.
Representative contemporary medical imaging methods like CT (computed tomography) and MRI (magnetic resonance imaging) have limitations in capturing fine vascular structures due to their constraints in resolution and sensitivity. Moreover, the use of contrast agents in these methods is restricted due to the potentially fatal side effects in patients with kidney disease. In contrast, ultrasound imaging, considered safe enough for fetal monitoring, utilizes the Doppler effect to measure real-time blood flow velocity and direction without the need for contrast agents. However, the current imaging speed has limitations in capturing fine blood vessels with sufficient sensitivity. The research team has enhanced microvascular sensitivity by employing ultrafast ultrasound acquisition capturing 1,000 frames per second, a speed over 100 times faster than conventional ultrasound imaging.
Using this technique, the researchers achieved a world-first by imaging the entire three-dimensional vascular network of renal artery, vein and 167μm (micrometer) thick interlobular arteries and veins in the renal cortex without the need for contrast agent. Furthermore, they conducted a continuous observation of renal vascular changes in an animal model induced with renal failure, performing multivariate analysis using hemodynamic and vascular morphological indicators. The results revealed a sharp decrease in renal blood flow during acute renal failure, while in the case of diabetic nephropathy, they identified chronic vascular degeneration in the kidneys accompanied by vascular distortion.
Professor Chulhong Kim explained, “The system allows us to understand the pathophysiology of diseases leading to kidney failure, enabling the observation of vascular changes before and after kidney transplantation.” He added, “It has significant potential to be used to study blood circulation and functional impairment across various organs including the digestive system, circulatory system, and cerebral nervous system.”
The research was supported by the National Research Foundation (NRF) grants, the Korea Medical Device Development Fund grant, the Korean Fund for Regenerative Medicine and BK21 FOUR projects (Pohang University of Science and Technology) funded by the Korean government (the Ministry of Science and ICT; the Ministry of Education; the Ministry of Trade, Industry and Energy; the Ministry of Health and Welfare).

Young adults who reported higher stress during their teenage years to adulthood were more likely to have high blood pressure, obesity and other cardiometabolic risk factors than their peers who reported less stress, according to new research published today in the Journal of the American Heart Association, an open access, peer-reviewed journal of the American Heart Association.
Cardiometabolic risk factors often occur together and are a significant cause of cardiovascular disease. These include obesity, Type 2 diabetes or prediabetes, high cholesterol and high blood pressure, researchers noted.
Understanding the effects of perceived stress starting in childhood is important for preventing, lessening or managing higher cardiometabolic risk factors in young adults,” said study author Fangqi Guo, Ph.D., postdoctoral research fellow at Keck School of Medicine, University of Southern California, Los Angeles.
“Our findings suggest that perceived stress patterns over time have a far-reaching effect on various cardiometabolic measures including fat distribution, vascular health and obesity,” Guo said. “This could highlight the importance of stress management as early as in adolescence as a health protective behavior.”
In 2020, cardiometabolic diseases, including cardiovascular diseases and Type 2 diabetes, were the most prevalent chronic health conditions and collectively accounted for nearly a quarter of all deaths in the U.S., according to the American Heart Association statistics. In 2023, the American Heart Association noted the strong connections among cardiovascular disease, kidney disease, Type 2 diabetes and obesity, and suggested redefining cardiovascular risk, prevention and management.
Childhood adversities affect cardiometabolic health across the life course, and interventions that improve early exposures may be more appropriate than interventions for cardiovascular disease risk factor effects later in life, according to a 2017 American Heart Association Scientific Statement: Childhood and Adolescent Adversity and Cardiometabolic Outcomes. In recent decades, researchers have found that perceived stress is a risk factor for cardiometabolic health conditions.
For this study, researchers analyzed health information from the Southern California Children’s Health Study. Participants had enrolled in the study as children along with their parents, then participated in follow-up assessments as adolescents — average age 13 — and as young adults — average age 24.

At each stage, stress was measured with a 4-item Perceived Stress Scale, a questionnaire about feelings and thoughts during the last month. Study participants were categorized into four risk-based groups: consistently high stress over time, decreasing stress over time, increasing stress over time and consistently low stress over time.
To evaluate cardiometabolic risk in young adulthood, Guo and colleagues used measures of carotid artery intima-media thickness (measures neck artery thickness); systolic (top number) and diastolic (bottom number) blood pressure; weight, percentage of body fat and fat distribution; and hemoglobin A1c. Hemoglobin A1c gauges blood sugar over time; increased thickness of the neck artery’s inner layers suggests blood may not be flowing smoothly; and more fat around the abdomen is associated with a higher risk of cardiovascular diseases and/or Type 2 diabetes.
The analysis found: Consistently high perceived stress from adolescence through adulthood was associated with greater risk for cardiometabolic diseases in young adulthood. If individuals experienced greater levels of stress from their teenage years into adulthood, they were more likely to have worse vascular health, higher total body fat, more fat around the belly and higher risk of obesity compared to those who felt less stressed over time. In general, higher perceived stress levels were also associated with higher risk for cardiometabolic health conditions. For example, adults who experience higher levels of stress tended to have worse vascular health and higher systolic and diastolic blood pressure.”Although we assumed that perceived stress patterns should have some association with cardiometabolic measures, we did not expect such consistent patterns across various risk factors,” Guo said.
“Health care professionals should consider using the Perceived Stress Scale to evaluate individuals’ stress levels during clinic visits. This way, those with higher stress levels can be identified and receive treatment earlier.”
Study details, background or design: Researchers reviewed data on 276 people from Southern California communities participating in the Southern California Children’s Health Study. Participants enrolled as children from 2003 to 2014 and took part in follow-up health assessments as adults from 2018 to 2021. About 56% of participants were girls/women; 62% identified as white; 5% as Asian; 1% as either Black or Native American; and 13% were classified as “other.” About 47% identified as Hispanic. Researchers investigated perceived stress reported by participants’ parents during childhood (average age of about 6 years); then by participants, themselves, in adolescence (average age about 13 years); and then again in young adulthood (average age nearly 24 years).A limitation was the study’s relatively small size. Studies with more participants would help clarify the results.