Study shows social factors of low U.S. Breast cancer screening

Photo Credit: Marco Jean deOliveira Teixeira

To identify major social factors hindering breast cancer screening in women aged 40 and older in the U.S., researchers focused on race/ethnicity, employment, education, food security, insurance status, housing and access to quality health care.

There is a pressing need to explore and understand which social determinants of health (SDOH) and health inequities act as significant influential factors that contribute to low breast cancer screening behaviors in the United States.

Health disparities have been consistently associated with delayed screening, which then contributes to higher mortality rates among both Hispanic and Black populations. Moreover, poverty, lack of education, neighborhood disadvantage, residential segregation, racial discrimination, lack of social support and social isolation also play a role in the breast cancer stage at diagnosis.

Researchers from Florida Atlantic University’s Schmidt College of Medicine conducted a scoping review of 72 peer-reviewed observational studies published between 2013 and 2023 to identify the major SDOH that hinder breast cancer screening in women aged 40 and older in the U.S. They focused on race/ethnicity, employment, education, food security, insurance status, housing and access to quality health care.

Low iron levels resulting from infection could be key trigger of long COVID

Photo Credit: Malachi Cowie

Problems with iron levels in the blood and the body’s ability to regulate this important nutrient as a result of SARS-CoV-2 infection could be a key trigger for long COVID, new research has discovered.

"Iron levels, and the way the body regulates iron, were disrupted early on during SARS-CoV-2 infection, and took a very long time to recover, particularly in those people who went on to report long COVID months later"

Aimee Hanson

The discovery not only points to possible ways to prevent or treat the condition, but could help explain why symptoms similar to those of long COVID are also commonly seen in a number of post-viral conditions and chronic inflammation.

Although estimates are highly variable, as many as three in 10 people infected with SARS-CoV-2 could go on to develop long COVID, with symptoms including fatigue, shortness of breath, muscle aches and problems with memory and concentration (‘brain fog’). An estimated 1.9 million people in the UK alone were experiencing self-reported long COVID as of March 2023, according to the Office of National Statistics.

Shortly after the start of the COVID-19 pandemic, researchers at the University of Cambridge began recruiting people who had tested positive for the virus for the COVID-19 cohort of the National Institute for Health and Care Research (NIHR) BioResource. These included asymptomatic healthcare staff identified via routine screening through patients admitted to Cambridge University Hospitals NHS Foundation Trust, and some to its intensive care unit.

A step toward personalized immunotherapy for all

This immunofluorescence image shows CD4+ (green) and CD8+ (yellow) T cells in the microenvironment of a head and neck squamous cell carcinoma.
Image Credit: Allen Lab, NCI/NIH.

Most cancers are thought to evade the immune system. These cancers don’t carry very many mutations, and they aren’t infiltrated by cancer-fighting immune cells. Scientists call these cancers immunologically “cold.”

Now new research suggests such cancers aren’t as “cold” as once thought. Researchers from the La Jolla Institute for Immunology (LJI), UC San Diego Moores Cancer Center, and UC San Diego, have found that patients with “cold” tumors actually do make cancer-fighting T cells.

This discovery opens the door to developing vaccines or therapies to increase T cell numbers and treat many more types of cancer than currently thought possible.

“In virtually every patient we’ve looked at, with every kind of cancer we’ve analyzed, we can detect pre-existing natural immunity against their tumor’s immunogenic subset of mutations known as neoantigens,” says LJI Professor Stephen Schoenberger, Ph.D., who co-led the new study with LJI Professor Bjoern Peters, Ph.D. “Therefore, we think these patients may actually benefit from empowering this response through personalized immunotherapy.”

“Every cancer patient is different,” adds Peters. “But this research is an important step toward finding immune cell targets relevant for individual patient tumors.”

Bariatric surgery provides long-term blood glucose control, type 2 diabetes remission

Photo Credit: Fernando Zhiminaicela

NIH-supported study shows long-term benefits of surgery compared to medication and lifestyle change.

People with type 2 diabetes who underwent bariatric surgery achieved better long-term blood glucose control compared to people who received medical management plus lifestyle interventions, according to a new study supported by the National Institutes of Health. The participants who underwent bariatric surgery, also called metabolic or weight-loss surgery, were also more likely to stop needing diabetes medications and had higher rates of diabetes remission up to 12 years post-surgery. Results of the study were published in JAMA and funded by the National institute of Diabetes, Digestive and Kidney Diseases (NIDDK), part of NIH.

“While there are many factors involved, and not all of them are completely understood, bariatric surgery typically results in greater weight loss that effects a person’s metabolic hormones, which improves the body’s response to insulin and ability to maintain healthy blood glucose levels,” said Dr. Jean Lawrence, NIDDK project scientist. “These results show that people with overweight or obesity and type 2 diabetes can make long-term, improvements in their health and change the trajectory of their diabetes through surgery.”

Immune system meets cancer: Checkpoint identified to fight solid tumor

Immunofluorescence image of the expression of PHGDH (red) and CD3 T cells (green) in cryosectioned AE17 mesothelioma.
Image Credit: Zhengnan Cai

Checkpoint PHDGH in tumor-associated macrophages influences immune response and tumor growth

A study by a scientific team from the University of Vienna and the MedUni Vienna, recently published in the top-class journal Cellular & Molecular Immunology, has a promising result from tumor research: The enzyme phosphoglycerate dehydrogenase (PHDGH) acts as a metabolic checkpoint in the function of tumor-associated macrophages (TAMs) and thus on tumor growth. Targeting PHGDH to modulate the cancer-fighting immune system could be a new starting point in cancer treatment and improve the effectiveness of clinical immunotherapies.

Our immune system constantly fights emerging cancer cells that arise from mutations. This process is controlled, among other things, by different types of macrophages. Tumor-associated macrophages (TAMs) are among the most abundant immune cells in the tumor microenvironment. They come from tissue-resident immune cells circulating in the blood that penetrate the tumor and differentiate there in response to various messenger substances (cytokines) and growth factors. In most solid tumors, TAMs are paradoxically considered to be tumor-promoting ("protumorigenic") overall: they promote tumor growth and metastasis by suppressing the immune response, promoting the vascular supply to the tumor and also increasing resistance to drug therapies – i.e. they generally correlate with a poor prognosis for the affected patients. Previous attempts to influence TAMs proved unsatisfactory because many patients had only a limited response to these therapeutic approaches. This underlines the urgency of finding new active ingredients and strategies.

Gut-brain communication turned on its axis

How the gut communicates with the brain
Image Credit: Copilot AI

The mechanisms by which antidepressants and other emotion-focused medications work could be reconsidered due to an important new breakthrough in the understanding of how the gut communicates with the brain.

New research led by Flinders University has uncovered major developments in understanding how the gut communicates with the brain, which could have a profound impact on the make-up and use of medications such as antidepressants.

“The gut-brain axis consists of complex bidirectional neural communication pathway between the brain and the gut, which links emotional and cognitive centers of the brain,” says Professor Nick Spencer from the College of Medicine and Public Health.

“As part of the gut-brain axis, vagal sensory nerves relay a variety of signals from the gut to the brain that play an important role in mental health and wellbeing.

“The mechanisms by which vagal sensory nerve endings in the gut wall are activated has been a major mystery but remains of great interest to medical science and potential treatments for mental health and wellbeing.”

Vaping can increase susceptibility to infection by SARS-CoV-2

UC Riverside study urges e-cigarette users to be cautious about vaping in the era of COVID-19
Photo Credit: Karl Edwards

Vapers are susceptible to infection by SARS-CoV-2, the virus that spreads COVID-19 and continues to infect people around the world, a University of California, Riverside, study has found.

The liquid used in electronic cigarettes, called e-liquid, typically contains nicotine, propylene glycol, vegetable glycerin, and flavor chemicals. The researchers found propylene glycol/vegetable glycerin alone or along with nicotine enhanced COVID-19 infection through different mechanisms.  

The researchers also found that the addition of benzoic acid to e-liquids prevents the infection caused by propylene glycol, vegetable glycerin, and nicotine. 

“Users who vape aerosols produced from propylene glycol/vegetable glycerin alone or e-liquids with a neutral to basic pH are more likely to be infected by the virus, while users who vape aerosols made from e-liquids with benzoic acid — an acidic pH — will have the same viral susceptibility as individuals who do not vape,” said Rattapol Phandthong, a postdoctoral researcher in the Department of Molecular, Cell and Systems Biology and the research paper’s first author.

The researchers obtained airway stem cells from human donors to produce a 3D tissue model of human bronchial epithelium. They then exposed the tissues to JUUL and BLU electronic cigarette aerosols to study the effect on SARS-CoV-2 infection. They found all tissues showed an increase in the amount of ACE2, a host cell receptor for the SARS-CoV-2 virus. Further, TMPRSS2, an enzyme essential for the virus to infect cells, was found to show increased activity in tissues exposed to aerosols with nicotine.

Arterial Connections Improve Treatment Outcomes Following Stroke

Visualization of the blood vessels in the brain of a patient without early venous filling, meaning without excessive reperfusion of the brain area after removal of the blood clot in the blocked artery.
Image Credit: P. Thurner und Z. Kulcsar, USZ

Blood vessels that cross-connect adjacent arterial trees regulate blood flow to the brain in stroke patients. Researchers at the University of Zurich have now shown that these vessels prevent brain hemorrhage following treatment to remove blood clots. They play a crucial role in the recovery of stroke patients.

Ischemic strokes are a major health burden. They occur when a blood vessel that supplies the brain becomes blocked, impairing blood flow to the brain. As a result, brain tissue suffers from a lack of oxygen and nutrients, which causes symptoms such as paralysis, confusion, dizziness, headache, trouble speaking or even death.

Many stroke patients recover poorly despite timely treatment

To treat these symptoms and restore blood flow to the brain, the obstructed vessel needs to be “declogged”, or recanalized. Contemporary treatments to remove the clot include intravenous thrombolysis or mechanical thrombectomy using a catheter. However, even with timely clot removal, many stroke patients only recover poorly.

The research group of Susanne Wegener, professor at the University of Zurich (UZH) and senior leading physician at the Department of Neurology of the University Hospital Zurich (USZ), has now demonstrated that the outcome of stroke treatments depends on the collateral network. Collaterals are blood vessels that cross-connect adjacent arterial trees, providing potential detour networks in case of a vascular blockage. “These vascular bridges maintain cerebral autoregulation and allow for a slower, gradual reperfusion, which results in smaller infarcts,” says Wegener.

Targeting inflammatory protein could help treat severe asthma

Image Credit: Copilot AI

Just weeks after news of a sharp national spike in asthma deaths – with South Australia recording the highest increase in a single year (88%) – scientists have revealed a promising new treatment for the chronic lung disease.

Australian researchers have found that a family of proinflammatory molecules called beta common cytokines control inflammation and scarring of the airways (fibrosis) in severe and steroid-resistant asthma.

They believe that a human therapeutic antibody called trabikihart could be the key to effectively blocking inflammation and scarring.

The findings, published in the Journal of Allergy and Clinical Immunology, are a result of a joint study led by researchers from the University of South Australia (UniSA) and the Royal Melbourne Institute of Technology (RMIT), in collaboration with researchers from CSL and SA Pathology.

Joint study leader Dr Damon Tumes, Head of the Allergy and Cancer Immunology Laboratory in the Centre for Cancer Biology*, says the findings are significant.

Antibody reduces allergic reactions to multiple foods in NIH clinical trial

Drug can help protect kids with multiple food allergies during accidental exposure.
Image Credit: Copilot AI

A 16-week course of a monoclonal antibody, omalizumab, increased the amount of peanut, tree nuts, egg, milk and wheat that multi-food allergic children as young as 1 year could consume without an allergic reaction in a late-stage clinical trial. Nearly 67% of participants who completed the antibody treatment could consume a single dose of 600 milligrams (mg) or more of peanut protein, equivalent to 2.5 peanuts, without a moderate or severe allergic reaction, in contrast with less than 7% of participants who received placebo. The treatment yielded similar outcomes for egg, milk, wheat, cashew, walnut and hazelnut at a threshold dose of 1,000 mg protein or more. This suggests the antibody therapy has the potential to protect children and adolescents if they accidentally eat a food to which they are allergic despite efforts to avoid it, according to the investigators. The findings were presented today at the American Academy of Allergy, Asthma & Immunology Annual Meeting in Washington, D.C., and published in The New England Journal of Medicine.

“People with food allergies and their caregivers need to maintain constant vigilance to avoid foods that could cause a potentially life-threatening allergic reaction. This is extremely stressful, especially for parents of young children,” said Jeanne Marrazzo, M.D., M.P.H., director of the National Institute of Allergy and Infectious Diseases (NIAID), part of the National Institutes of Health and the trial’s regulatory sponsor. “Although food avoidance remains critical, the findings reported today show that a medicine can help reduce the risk of allergic reactions to common foods and may provide protection from accidental exposure emergencies.”

Outsmarting chemo-resistant ovarian cancer

Ovarian Tumor Microenvironment
Image Credit: National Cancer Institute

New approach with nanoparticle starves cells of cholesterol and reduces tumor growth by 50%

Treatment with the nanoparticle reduced ovarian tumor growth by more than 50% in human cells and animal models.

Women diagnosed with ovarian cancer may initially respond well to chemotherapy, but the majority of them will develop resistance to treatment and die from the disease.

Now Northwestern Medicine scientists have discovered the Achilles heel of chemotherapy-resistant ovarian cancer — its hunger for cholesterol — and how to sneakily use that to destroy it.

In a new study, scientists first showed that chemotherapy-resistant ovarian cancer cells and tumors are rich in cholesterol due to an increased uptake of it. They then deployed a synthetic nanoparticle that appeared to the cancer cells as a natural one rich in cholesterol. But when the cancer cells bound the fake particle, the mimic actually blocked cholesterol uptake. Additionally, the scientists showed that reducing cholesterol tricked the cancer cells down a cell death pathway. Treatment with the nanoparticle reduced ovarian tumor growth by more than 50% in human cells and animal models.

Anti-diabetic drugs could lower risk of primary and secondary brain cancer

Photo Credit: Tesa Robbins

Diabetic patients who take anti-diabetic drugs - known as glitazones – long term had a lower risk of primary and secondary brain cancer compared with diabetic patients on other medications, new research led by the University of Bristol has found.

The study, published in BMJ Open, suggests these drugs could be repurposed to prevent brain metastasis in cancer patients who are at high risk of secondary cancers, if the current research is supported by future studies.

PPAR- α agonists (fibrates) and PPAR γ agonists (glitazones) drugs are clinically important due to their widespread safe use to treat high cholesterol (hyperlipidemia) and diabetes.  Previous studies have suggested that fibrates and glitazones may have a role in brain tumor prevention. Given the drug's safety and cost, they have the potential to be repurposed to prevent brain cancers and reduce the risk of secondary tumors by stopping tumor growth.

Using primary care records from the UK GP database Clinical Practice Research Datalink (CPRD), which contains data from a network of over 2,000 GPs from more than 670 practices across the UK, the researchers examined if this theory could be supported.

Mice study suggests metabolic diseases may be driven by gut microbiome, loss of ovarian hormones

Mice that received fecal implants from donors that had their ovaries removed gained more fat mass and had greater expression of liver genes associated with inflammation, Type 2 diabetes, fatty liver disease and atherosclerosis. The findings may shed light on the greater incidence of metabolic dysfunction in postmenopausal women. The team members included, from left: molecular and integrative physiology professor Erik R. Nelson; Kelly Swanson, the director of the Division of Nutritional Sciences and the Kraft Heinz Endowed Professor in Human Nutrition; and animal sciences professor Brett R. Loman.
  Photo Credit: Fred Zwicky

The gut microbiome interacts with the loss of female sex hormones to exacerbate metabolic disease, including weight gain, fat in the liver and the expression of genes linked with inflammation, researchers found in a new rodent study.

The findings, published in the journal Gut Microbes, may shed light on why women are at significantly greater risk of metabolic diseases such as obesity and Type 2 diabetes after menopause, when ovarian production of female sex hormones diminishes.

“Collectively, the findings demonstrate that removal of the ovaries and female hormones led to increased permeability and inflammation of the gut and metabolic organs, and the high-fat diet exacerbated these conditions,” said Kelly S. Swanson, the director of the Division of Nutritional Sciences and the Kraft Heinz Endowed Professor in Human Nutrition at the University of Illinois Urbana-Champaign who is a corresponding author of the paper.  “The results indicated that the gut microbiome responds to changes in female hormones and worsens metabolic dysfunction.”

Stopping the awakening of leukemia stem cells to prevent relapse

Acute Myeloid Leukemia
Image Credit: National Cancer Institute

Why myeloid leukemias start to grow again after chemotherapy has killed the bulk of cancerous cells, and how growth may be blocked by repurposed drugs, may have been solved by new research.

The bone marrow of Acute Myeloid Leukemia (AML) patients contains a rare population of leukemic stem cells (LSCs) that do not grow and, therefore, are not killed by chemotherapy.

However, after treatment, these cells start to grow and produce AML cells, but it has until now been unclear as to what kick-starts this process.

In a new study, published in Nature Communications, experts from Newcastle University, the University of Birmingham and the Princess Maxima Centre of Pediatric oncology, studied single cells from patients with t(8;21) AML to investigate what made the rare LSCs grow.

Long COVID linked to persistently high levels of inflammatory protein: a potential biomarker and target for treatments

"We hope that this could help to pave the way to develop therapies and give some patients a firm diagnosis," -Benjamin Krishna
Photo Credit: Annie Spratt

SARS-CoV-2 triggers the production of the antiviral protein IFN-γ, which is associated with fatigue, muscle ache and depression. New research shows that in Long COVID patients, IFN-y production persists until symptoms improve, highlighting a potential biomarker and a target for therapies.

A University of Cambridge-led study identifies the protein interferon gamma (IFN-γ) as a potential biomarker for Long COVID fatigue and highlights an immunological mechanism underlying the disease, which could pave the way for the development of much needed therapies, and provide a head start in the event of a future coronavirus pandemic. 

The study, published today in Science Advances, followed a group of patients with Long COVID fatigue for over 2.5 years, to understand why some recovered and others did not. 

Long COVID continues to affect millions of people globally and is placing a major burden on health services. An estimated 1.9 million people in the UK alone (2.9% of the population) were experiencing self-reported Long COVID as of March 2023, according to the ONS. Fatigue remains by far the most common and debilitating symptom and patients are still waiting for an effective treatment.

Researchers reveal mechanism of drug reactivating tumor suppressors

Mechanism of methylated-histone inhibitor valemetostat
Researchers revealed the mechanism of the cancer drug valemetostat and established its efficacy in treating adult T-cell leukemia/lymphoma (ATL).
Illustration Credit: ©2024 Makoto Yamagishi, The University of Tokyo

Researchers have revealed the mechanism of a drug shown to be effective in treating certain types of cancer, which targets a protein modification silencing the expression of multiple tumor suppressor genes. They also demonstrated in clinical trials the efficacy of the drug in reducing tumor growth in blood cancer. The findings could lead to longer-term treatments for the disease and therapies for other types of cancer with similar underlying causes.

A team of researchers from the University of Tokyo and their collaborators focused on therapies targeting H3K27me3, a modification on a DNA-packaging histone protein, which plays a large role in regulating gene expression. The modification occurs when methyl groups, each consisting of three hydrogen atoms bonded to a single carbon atom (CH3), are added to the protein in a process called methylation.

The modification, also referred to as being epigenetic (a heritable change in gene function that occurs without altering the sequence of the DNA), has been tied to the repression, or reducing the expression, of tumor suppressor genes, with the accumulation of the methylated histones around the genes.

Possible trigger for autoimmune diseases discovered

 One of the great mysteries of immunology: the function of B cells (green) in the thymus gland was previously unknown. Researchers have now been able to show that the immune cells help to prevent T cells from attacking the body.
Image Credit: Jan Böttcher, Thomas Korn / TUM

Immune cells must learn not to attack the body itself. A team of researchers from the Technical University of Munich (TUM) and the Ludwig Maximilian University of Munich (LMU) has discovered a previously unknown mechanism behind this: other immune cells, the B cells, contribute to the "training" of the T cells in the thymus gland. If this process fails, autoimmune diseases can develop.

In children and adolescents, the thymus gland functions as a "school for T cells". The organ in our chest is where the precursors of those T cells that would later attack the body's own cells are discarded. Epithelial cells in the thymus present a large number of molecules that occur in the body to the future T cells. If any of them reacts to one of these molecules, a self-destruction program is triggered. T cells that attack the body's own molecules remaining intact and multiplying, on the other hand, can cause autoimmune diseases.

New mechanism discovered

In Nature, the team led by Thomas Korn, Professor of Experimental Neuroimmunology at TUM and a Principal Investigator in the SyNergy Cluster of Excellence, and Ludger Klein, Professor of Immunology at LMU’s Biomedical Center (BMC), describe another previously unknown mechanism behind this.

In addition to the precursors of T cells, the thymus gland also contains other immune cells, the B cells. They develop in the bone marrow but migrate to the thymus in early childhood. "The function of B cells in the thymus gland has been a mystery that has puzzled immunologists for many years," says Thomas Korn. The researchers have now been able to show for the first time that B cells play an active role in teaching T cells which targets not to attack.

False Alarm of the Immune System during Muscle Disease

Prof. Claudia Günther (left) from Dresden and Prof. Eva Bartok (right) from Bonn are jointly investigating the connection between myotonic dystrophy and autoimmune diseases.
Photo Credit: © Universitätsklinikum Dresden & Universitätsklinikum Bonn

Researchers at the University Hospitals of Dresden and Bonn of the DFG Transregio 237 and from the Cluster of Excellence ImmunoSensation2 at the University of Bonn have made progress clarifying why patients with myotonic dystrophy 2 have a higher tendency to develop autoimmune diseases. Their goal is to understand the development of the disease, and their research has provided new, potential therapeutic targets. The results of the study have now been published in the renowned journal Nature Communications.

Myotonic dystrophy 2 (DM2) is a form of muscular dystrophy, a disease that leads to progressive muscle degeneration. It is caused by the expansion of a repetitive DNA sequence containing multiple CCTG bases in the CNBP gene. In general, the sequence of nucleobases in the DNA carries the genetic information. Patients suffer from muscle weakness that is more pronounced in the area of the muscles close to the trunk, as well as sustained muscle stiffness and pain. Although DM2 occurs in roughly one out of 10,000 people in Germany, there are no targeted therapies. In initial studies, Prof. Claudia Günther and her team at the Carl Gustav Carus University Hospital at the Technical University of Dresden also observed that patients with DM2 suffer more from autoimmune diseases with an increased production of antibodies in the blood than the general population. However, the underlying mechanism for these symptoms was previously unknown.

NIH study offers new clues into the causes of post-infectious ME/CFS

In-depth study finds brain, immune, and metabolic abnormalities linked to debilitating chronic disease.
Image Credit: John A Beal
(CC BY 4.0 DEED)

In a detailed clinical study, researchers at the National Institutes of Health have found differences in the brains and immune systems of people with post-infectious myalgic encephalomyelitis/chronic fatigue syndrome (PI-ME/CFS). They also found distinct differences between men and women with the disease. The findings were published in Nature Communications.

“People with ME/CFS have very real and disabling symptoms, but uncovering their biological basis has been extremely difficult,” said Walter Koroshetz, M.D., director of NIH’s National Institute of Neurological Disorders and Stroke (NINDS). “This in-depth study of a small group of people found a number of factors that likely contribute to their ME/CFS. Now researchers can test whether these findings apply to a larger patient group and move towards identifying treatments that target core drivers of the disease.”

A team of multidisciplinary researchers discovered how feelings of fatigue are processed in the brains of people with ME/CFS. Results from functional magnetic resonance imaging (fMRI) brain scans showed that people with ME/CFS had lower activity in a brain region called the temporal-parietal junction (TPJ), which may cause fatigue by disrupting the way the brain decides how to exert effort.

They also analyzed spinal fluid collected from participants and found abnormally low levels of catecholamines and other molecules that help regulate the nervous system in people with ME/CFS compared to healthy controls. Reduced levels of certain catecholamines were associated with worse motor performance, effort-related behaviors, and cognitive symptoms. These findings, for the first time, suggest a link between specific abnormalities or imbalances in the brain and ME/CFS.

Mitochondrial activation in transplanted cells promotes regenerative therapy for heart healing

Regenerative therapy to treat heart failure is more effective when the mitochondria of the regenerative cells are activated prior to treatment.
Image Credit: Gemini Advance

Heart failure stands as a leading cause of mortality worldwide, demanding advanced treatment options. Despite the urgency for more effective treatments, options for severe heart failure remain limited. Cell transplantation therapy has emerged as a promising ray of hope, as it can be used in regenerative therapy to heal the heart.

A research team led by Professor Yuma Yamada of Hokkaido University’s Faculty of Pharmaceutical Science has developed a technique to promote cardiac regeneration by delivering mitochondrial activators to cardiac progenitor cells. Their findings were published in the Journal of Controlled Release.

“Cardiomyocytes efficiently use the mitochondrial tricarboxylic acid cycle to produce large amounts of adenosine triphosphate from several substrates via oxidative phosphorylation (OXPHOS),” explains Yamada. “Based on the energy metabolism of cardiomyocytes, we hypothesized that activating the mitochondrial function of transplanted cells may improve the outcome of cell transplantation therapy.”