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Under the direction of Boyd Professor Nicolas Bazan, MD, PhD, scientists at LSU Health New Orleans Neuroscience Center of Excellence have developed a new, experimental human cell line from retinal pigment epithelial cells. Called ABC, these cells so closely resemble and retain the properties of native retinal pigment epithelial (RPE) cells, the research team has shown that they are a reliable cell system to study retinal degenerative diseases. Their findings are published in Frontiers in Neuroscience.
Retinal pigment epithelial (RPE) cells serve as part of a blood/retina barrier. They protect the integrity of photoreceptor cells critical to vision.
“Retinal pigment epithelial cells and photoreceptor cells are at constant risk for uncompensated oxidative stress because of their oxygen-rich environment, high flux of polyunsaturated fatty acids and high metabolic activity,” notes Dr. Bazan. “Impairments in RPE cell protection may lead to retinal degenerative diseases, including age-related macular degeneration (AMD).”
The new cell has allowed the study of events relevant to the biology involved in the normal repair process, which eliminates cell structures damaged by oxidative stress.
“This new cell line also facilitates the search for mechanisms of senescence gene programming and the unraveling of the relationship between these mechanisms in the normal cycle of a cell for neuroprotection and cell survival,” Bazan adds.
According to the Library of Medicine, “Age-related macular degeneration (AMD) is the most common cause of blindness prevalent in developed countries, particularly in people older than 60 years. It accounts for 8.7% of all types of blindness worldwide.
There may be additional benefits of this new cell line.
“RPE cells also share features with brain cells,” says Bazan, who is also the inaugural founder of the Ernest C. and Yvette C. Villere Chair for Retinal Degenerative Diseases. “This similarity is currently being used to convert RPE cells into photoreceptors for cellular replacement therapies in blinding eye diseases, and the new cell would be a good candidate for that purpose. This cell line may also be used to more precisely uncover the fundamental mechanisms of neurodegenerative diseases such as Alzheimer’s.”
This work was supported by the National Institutes of Health (NIH)/National Eye Institute (NEI) grant R01 EY005121 and the Eye Ear Nose & Throat (EENT) Foundation of New Orleans.
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As most Americans wind down for bed, 15 million people are just clocking into work. These hospital workers, emergency responders, factory operators and others are among the 20 percent of the world’s population who do shift work. Their different sleep-wake cycle elevates their risk for numerous health disorders, including diabetes, heart attacks, cancer and strokes.
Now, new research published in Neurobiology of Sleep and Circadian Rhythms shows the adverse effects of shift work can be long-lasting, even after returning to a normal schedule.
“Shift work, especially rotating shift work, confuses our body clocks and that has important ramifications in terms of our health and well-being and connection to human disease,” said David Earnest, professor in the Department of Neuroscience and Experimental Therapeutics at the Texas A&M University College of Medicine. “When our internal body clocks are synchronized properly, they coordinate all our biological processes to occur at the right time of day or night. When our body clocks are misaligned, whether through shift work or other disruptions, that provides for changes in physiology, biochemical processes and various behaviors.”
A previous study done by Earnest and colleagues found animal models on rotating shift work schedules had more severe stroke outcomes, in terms of both brain damage and functional deficits, than those on regular 24-hour cycles of day and night. Males were distinguished by worse outcomes in which mortality rates were much higher.
This new study took a different approach. Rather than examining immediate effects of shift work on strokes, the researchers returned all subjects to regular 24-hour cycles and waited until their midlife equivalent — when humans are most likely to experience a stroke — to evaluate stroke severity and outcomes.
“What was already born out in epidemiological studies is that most people only experience shift work for five to eight years and then presumably go back to normal work schedules,” Earnest said. “We wanted to determine, is that enough to erase any problems that these circadian rhythm disruptions have, or do these effects carry over even after returning to normal work schedules?”
They found that the health impacts of shift work do, indeed, persist over time. The sleep-wake cycles of subjects on shift work schedules never truly returned to normal, even after subsequent exposure to a regular schedule. Compared to controls maintained on a regular day-night cycle throughout the study, they displayed persistent alterations of their sleep-wake rhythms, with periods of abnormal activity when sleep would have normally occurred. When they suffered strokes, their outcomes were again much worse than the control group, except females had more severe functional deficits and higher mortality than the males.

Patients with heart disease are at risk of experiencing a potentially lethal “electrical storm” involving recurrent episodes of a type of irregular heartbeat called ventricular tachycardia (VT).
Electric shock therapy is used to treat VT following a heart attack, but unfortunately, options to prevent its recurrence are limited.
New research led by investigators at Massachusetts General Hospital (MGH) reveals that two different white blood cell types influence VT in the heart, suggesting that treatments that influence these cells may help reduce patients’ risk of sudden cardiac death.
The work, which is published in Nature Cardiovascular Research, is based on the knowledge that cardiac conditions (such as heart attacks) that increase the risk of VT and other heartbeat irregularities lead to massive changes in the white blood cell populations surrounding the heart.
To study the mechanisms involved, MGH scientists developed a new research model. “It was believed that mice don’t get VT after a heart attack, but we discovered a surprisingly simple trick to induce it — feeding mice food with low potassium levels,” says senior author Matthias Nahrendorf, MD, PhD, an investigator in MGH’s Center for Systems Biology, Professor of Radiology at Harvard Medical School, and the Richard Moerschner Endowed MGH Research Institute Chair in Men’s Health
“This is a major step forward because now we can study how different white blood cell subclasses influence heart rhythms. It is also clinically relevant because every fifth patient who experiences a heart attack has low blood potassium levels, and these patients are known to be particularly likely to develop heartbeat irregularities, or arrhythmia.”
The team’s experiments demonstrated that among the different white blood cell types, neutrophils promote VT while macrophages protect against it. “Inflammatory neutrophils give rise to arrhythmia by compromising the electrical function of heart muscle cells called cardiomyocytes,” explains Nahrendorf.
“Macrophages, which take up debris, are protective, and deleting them gave rise to electrical storm in mice with low potassium levels who experienced a heart attack. Indeed, these mice were more likely to die from arrhythmia.”
The findings indicate that additional research into the roles of white blood cells in arrhythmia could lead to new targeted therapies for irregular heart rhythms.
Funding for the study was provided by the NHLBI grants HL139598, HL142494, HL125428, HL155097.
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Brain function, much like many other areas of life, is all about balance. Excitatory neurons that increase the activity of connected neurons are balanced by inhibitory neurons that dampen this activity. In this way, excitation and inhibition work together throughout the brain to process information and guide behavior. An imbalance of these systems, which can sometimes arise during development, contributes to neurodevelopmental disorders such as autism. Until recently researchers have mostly focused on excitatory neurons, while the function and development of inhibitory neuronal circuits has been understudied.
New research from the Max Planck Florida Institute for Neuroscience demonstrates that inhibitory and excitatory neuronal circuits of the visual system develop through different processes, even if the organization of the mature circuit is similar. These findings, published in Nature Communications highlight the importance of the continued study of the development of these two systems, the understanding of which is fundamental to comprehending neurodevelopmental disorders.
An area of the brain that processes visual information, the primary visual cortex, is highly organized, forming patches of neighboring neurons that tend to be active together and respond to similar visual features. In mammals, these modular functional maps consist of both excitatory and inhibitory neurons that work together to create an accurate representation of the world.
Scientists Jeremy Chang and David Fitzpatrick have now characterized the development of these functional maps for inhibitory neurons in primary visual cortex. Although excitatory and inhibitory functional maps are matched at maturity, their development occurs through different parallel processes.
Excitatory neurons show modular organization early on, before the eyes open and visual input is received. Neighboring neurons respond to visual images in a correlated fashion and show similar preferences for stimuli presented in specific orientations. While visual experience refines particular properties of these maps, such as the alignment of visual information from each eye, the basic features of the modular organization are present before visual experience.
Dr. Chang found that inhibitory neurons, on the other hand, lack much of this modular activity before visual experience. “This came as a surprise,” he admitted. “We were not expecting the functional maps seen before eye-opening in excitatory neurons to be almost absent in inhibitory neurons.” This suggested that developing mature functional organization of inhibitory neurons requires visual experience. In fact, if visual input was delayed, the development of many features of the functional inhibitory neuron maps was also delayed.
This work contributes to the fundamental understanding of larger questions about the role of inhibition in the cortex, which the lab will continue to pursue. “New techniques developed over the last decade have allowed us to image the activity of inhibitory neurons in response to visual images. We are beginning to understand the functional importance of inhibition in visual processing and how the role of inhibition changes throughout development. During development, inhibitory and excitatory neurons have to solve different puzzles to end up in the correct place, connect to the appropriate partners, and refine their connections in response to experience,” said Chang. Future work will focus on understanding how these puzzles are solved.
This research was supported by the National Eye Institute of the National Institutes of Health under award numbers EY011488 and EY026273 and the Max Planck Florida Institute for Neuroscience. This content is solely the responsibility of the authors and does not necessarily represent the official views of the funders.
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The emotional context in which eating occurs has been thought to influence eating patterns and diet, with studies finding negative emotions predict excessive calorie intake and poor diet quality. A research article featured in the Journal of Nutrition Education and Behavior, published by Elsevier, discusses how children’s unhealthy food choices, especially over weekends, are related to emotion.
“Children are more likely to consume unhealthy foods on weekends when meals and snacks are less structured and supervised than on school days,” said Christine Hotaru Naya, MPH, Department of Population and Public Health Sciences, University of Southern California, Los Angeles, CA, USA. “We also focused on snack choices where children often make their own decisions.”
This study sampled 195 ethnically diverse children currently in third through sixth grades who lived in the greater Los Angeles metropolitan area. Children used a mobile phone app and were contacted seven times per day to answer questions. When contacted, they were asked if they were feeling stressed, mad or sad and to report if they had made any unhealthy eating choices from among fried foods, sweets, and sugary beverages over the previous two hours.
Across all food types sampled, sweet food consumption was reported the most often. Children reported eating sweets or pastries at least once daily on 40% of the days. Chips or fries were eaten at least once a day on nearly 30% of days, and sugar-sweetened beverages were consumed at least once per day on 25% of days.
The researchers also identified three negative mood patterns during a day: stable low; early increasing and late decreasing; and early decreasing and late increasing. In the study, on 90% of the days, children reported stable low negative mood, but the reminder had varying moods throughout the day.
“We found fried food consumption to be higher on days with more variable emotional patterns than days with consistent low negative mood,” says Naya. “These results align with other studies that have found the negative mood to positively predict children’s fatty food intake.” Sweet food and soda consumption did not follow the same patterns in this study.
Coauthor Daniel Chu, MPH, Department of Population and Public Health Sciences, University of Southern California, Los Angeles, CA, USA, notes, “This study has several strengths, including the ability to be repeated in the family home, and we were able to test a population of healthy children so results can be widely applied.”
These findings add to the evidence for incorporating mood and emotion-based components into interventions aiming to improve children’s dietary outcomes and eating behaviors. Specifically, results highlight mornings and evenings as two possible vulnerable periods when the change in negative emotions could influence food choices.
“More studies are needed for us to understand the relationship between a child’s emotions and their food choices, but this is a good start on that path to recognizing how to approach food choices with a person’s mood and emotions in mind,” concludes Naya. “We could improve our current interventions to be individually tailored to the environmental, social, emotional, and cognitive contexts in which unhealthy eating occurs.”
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The largest medical record-based study ever of adverse events suffered by hospitalized patients in the U.S., published in the July 12 issue of JAMA, reports a significant decrease in the rate of adverse events over the last decade. The study findings hold promise for both the safety of patients and the effectiveness of hospital patient safety initiatives.
In this study, the de-identified medical records of 244,542 patients across 3,156 U.S. hospitals over 10 years were examined. Researchers used the Medicare Patient Safety Monitoring System (MPSMS), a surveillance system managed by the Agency for Healthcare Research and Quality (AHRQ) designed to assess 21 in-hospital adverse events in patients with the key conditions of acute myocardial infarction (heart attack), heart failure, pneumonia, major surgical procedures, and all other conditions. Relative risks were adjusted for patient age, sex, race ethnicity, specific comorbidities, and each hospital’s characteristics.
The researchers report the rate of adverse events declined significantly between 2010 and 2019 in patients admitted for acute myocardial infarction, heart failure, pneumonia, and major surgical procedures. Some of the adverse events captured included adverse drug events, hospital-acquired infections, procedural complications, pressure ulcers and falls.
“Our study is the biggest and most comprehensive assessment of adverse events in patients hospitalized in the U.S. that is based on detailed analysis of the medical record as opposed to billing data, which can be misleading,” said co-author Dr. Mark Metersky, professor of medicine at UConn School of Medicine and chief of the Division of Pulmonary, Critical Care and Sleep Medicine at UConn Health. “There has been an improvement in patient safety in U.S. hospitals during the 10 years we studied. Our data shows that the major safety improvement efforts made by our country and our hospitals seems to be paying off.”
Researchers evaluated the in-hospital trends in the number of adverse events per 1,000 hospitalizations. For example, adverse events among patients who experienced heart attacks declined significantly over a decade from 218 in 2010 to 139 per 1,000 discharges in 2019; in heart failure patients, adverse events dropped from 168 to 116; in pneumonia patients from 195 to 119; and in major surgery patients, from 204 to 130. However, for those with other conditions there was no observed change in the number of adverse events in the same time period; however, reductions were seen in the first four groups and this fifth group as well when comorbidities and other factors, such as the age of patients, were taken into account.
Interestingly, the researchers observed larger improvements in the adverse event rate in older patients than younger ones, and there were few apparent differences in risk based on a patient’s race, ethnicity, sex or region of care in the U.S. All groups saw similar reductions. However, those patients who experienced adverse events throughout the period of study had substantially higher mortality rates and longer lengths of stays than those that did not experience an adverse event.
This study was funded by the AHRQ and the Centers for Medicare and Medicaid Services (CMS). At AHRQ, the collaborative research work was led by Noel Eldridge, who was the first author on the paper. Metersky from UConn is the clinical lead for the MPSMS and was a co-author along with a collaboration of researchers from Yale, CMS, the Federal ONC, Harvard, and others.
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Patients with a specific form of age-related macular degeneration (AMD), a leading cause of blindness in the United States, are at significant risk for cardiovascular disease and stroke, according to new research from New York Eye and Ear Infirmary of Mount Sinai. This study, published in the July issue of Retina, is the first to demonstrate a link between the disorders.
“For the last three decades researchers have suggested an association between AMD and cardiovascular disease, but there has been no conclusive data on this until now. Our retinal team answered this important question by focusing on two different varieties of AMD that can be seen with advanced retinal imaging. We discovered that only one form of AMD, that with subretinal drusenoid deposits, is tightly connected to high-risk vascular diseases, and the other form, known as drusen, is not,” explains lead author R.Theodore Smith, MD, PhD, Professor of Ophthalmology at the Icahn School of Medicine at Mount Sinai. “If ophthalmologists diagnose or treat someone with the specific subretinal drusenoid deposits form of AMD, but who otherwise seems well, that patient may have significant undetected heart disease, or possibly carotid artery stenosis that could result in a stroke. We foresee that in the future, as an improved standard of care, such patients will be considered for early referral to a cardiologist for evaluation and possibly treatment.”
AMD is the leading cause of visual impairment and blindness in people over 65 years old and is the result of damage to the central area of the retina called the macula, which is responsible for reading and driving vision. One major form of early AMD is called drusen, where small yellow cholesterol deposits form in a layer under the retina. They can deprive the retina of blood and oxygen, leading to vision loss. Drusen formation can be slowed by appropriate vitamin supplementation.
The other major form of early AMD is the presence of subretinal drusenoid deposits (SDD), which is lesser known, and requires high-tech retinal imaging to detect. These deposits are also made of fatty lipids and other materials, but form in a different layer beneath the light sensitive retina cells, where they are also associated with vision loss. Currently, there is no known treatment for SDD.
Mount Sinai researchers analyzed 126 patients with AMD, using optical coherence tomography (OCT) — an advanced imaging system that provides high-resolution cross-sectional scans of the retina. Patients also answered questionnaires about their health history including heart disease and stroke. Of the patients on the study, 62 had SDD and 64 had drusen; 51 of the 126 total patients (40 percent) reported having cardiovascular disease or a past stroke, and most (66 percent) of those patients had SDD. By contrast, of the 75 patients who did not have known heart disease or stroke, relatively few (19 percent) had SDD. In statistical terms, patients with cardiovascular disease or stroke were three times more likely to have SDD than patients without.
The researchers suggested that the underlying heart and vascular disease likely compromises blood circulation in the eye, leading to the SDDs beneath the retina and ultimately causing vision loss and blindness.
“We believe poor ocular circulation that causes SDDs is a manifestation of underlying vascular disease. This has important public health implications and can facilitate population screening and disease detection with major impact,” explains author Jagat Narula, MD, PhD, Associate Dean of Global Affairs and Professor of Medicine (Cardiology), and Radiology, at the Icahn School of Medicine at Mount Sinai. “Seen in an eye clinic, such patients should be prompted to see a cardiologist. On the other hand, if clinically substantiated in prospective studies, SDDs could emerge as a risk marker for underlying vascular disease in asymptomatic patients in primary care or a cardiology clinic. The temporal relationship between SDDs and macrovascular disease will also need to be established in prospective studies which are currently in progress.”
Researchers also collected patient blood samples, and results show genetic risk factors may also play a role in SDD cases in addition to vascular causes. Specifically, they found that the ARMS2 gene acted independently of vascular disease to cause SDD in some patients.
“This study further demonstrates that AMD is not a single condition or an isolated disease, but is often a signal of systemic malfunction which could benefit from targeted medical evaluation in addition to localized eye care,” says Richard B. Rosen, MD, Chief of the Retina Service for the Mount Sinai Health System. “It helps bring us one step closer to unraveling the mystery of this horrible condition which robs so many patients of the pleasure of good vision during their later years. ”
This study was funded by Regeneron Pharmaceuticals Investigator-Initiated Study, Research to Prevent Blindness Challenge Grant, Macula Foundation, Bayer-Global Ophthalmology Award, and International Council of Ophthalmology-Alcon Fellowship.

The smaller plastic particles are, the more easily they can be taken up by cells. In addition, the shape, surface and chemical properties play an important role in answering the question of how the particles could affect human tissue. This is the result of a study by researchers at the German Federal Institute for Risk Assessment (BfR), published in the journal Microplastics and Nanoplastics.
“With this study, we want to help to close the still rather large knowledge gaps in the topic of health effects of ‘nanoplastics,'” says Dr. Holger Sieg, head of the research project. “However, these are laboratory experiments with cell cultures that cannot simply be transferred to humans.”
Plastic particles enter the environment from weathering and decaying polymer materials, car tyre or clothing abrasion and many other sources. As a result, various types of microplastic particles can be inhaled or ingested with drinks and food.
According to current knowledge, microplastics are considered to pose a comparatively low risk to human health. It is between one micrometre (millionth of a metre, unit µm) and five millimetres (thousandth of a metre, unit mm) in size and thus too “bulky” to be absorbed by human cells to any significant extent and distributed in the body. It is indigestible and is largely excreted again.
Nanoplastics can enter the cells
The situation is different with smaller particles, submicro- and nano-plastics. These particles are between one nanometre (billionth of a metre, unit nm) and 1000 nanometres (equivalent to one micrometre) in size. It is not yet known for sure whether and to which quantities they can enter the human body.
Holger Sieg and his team worked on submicrometre and nanoplastic particles and their effects on human small intestine and liver cells. Because these particles are so small and difficult to study, it is not easy to gain reliable insights into their effects on human tissue. The BfR team used various microscopy and testing methods to do this. The cells were exposed to various plastic types that are used in plastic tableware and cutlery or in food packaging.
Intestinal mucosa absorbs only few microparticles
It turned out that the smaller the particles, the more they were absorbed. The type of particles also played an important role. The cells of the small intestine, as a natural barrier between the intestinal contents and the organism, proved to be rather resistant. Microplastics only “seeped” into the cell to a small extent. The even smaller particles in the submicrometre range, on the other hand, could be measured in larger quantities in intestinal and liver cells. The particles either attached themselves directly to the cell membranes or were trapped in small bubbles of cell membrane, a process known as endocytosis.
It is not yet clear whether such artificial inclusions can disrupt the normal metabolism of the cell. Plastic particles could also bind potentially harmful substances to themselves and introduce them into the cell as a “Trojan horse.” Possible effects of submicrometre and nanoplastics are discussed, for example inflammatory effects. It will be investigated in further studies, to which extent this is the case.
“Although we worked in the laboratory with a model system that can only represent reality in a very simplified way, our findings can help to close gaps in our knowledge about the behaviour of the smallest plastic particles,” summarises BfR expert Holger Sieg. “However, it is not yet possible to say, whether the results are also valid for humans. For this, the laboratory findings must be verified in follow-up experiments.”
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Immunotherapy is a new cancer treatment that activates the body’s immune system to fight against cancer cells without using chemotherapy or radiotherapy. It has fewer side effects than conventional anticancer drugs because it attacks only cancer cells using the body’s immune system. In addition, because it uses the memory and adaptability of the immune system, patients who have benefited from its therapeutic effects experience sustained anticancer effects.
The recently developed immune checkpoint inhibitor has considerably improved the survival rate of patients with cancer. However, the problem with cancer immunotherapy is that only approximately 30% of cancer patients receive benefits from its therapeutic effect, and the current diagnostic techniques do not accurately predict the patient’s response to the treatment.
Under this circumstance, the research team led by Professor Sanguk Kim (Department of Life Sciences) at POSTECH is gaining attention as they have improved the accuracy of predicting patient response to immune checkpoint inhibitors (ICIs) by using network-based machine learning. The research team discovered new network-based biomarkers by analyzing the clinical results of more than 700 patients with three different cancers (melanoma, gastric cancer, and bladder cancer) and the transcriptome data of the patients’ cancer tissues. By utilizing the network-based biomarkers, the team successfully developed artificial intelligence that could predict the response to anticancer treatment. The team further proved that the treatment response prediction based on the newly discovered biomarkers was superior to that based on conventional anticancer treatment biomarkers including immunotherapy targets and tumor microenvironment markers.
In their previous study, the research team had developed machine learning that could predict drug responses to chemotherapy in patients with gastric or bladder cancer. This study has shown that artificial intelligence using the interactions between genes in a biological network could successfully predict the patient response to not only chemotherapy, but also immunotherapy in multiple cancer types.
This study helps detect patients who will respond to immunotherapy in advance and establish treatment plans, resulting in customized precision medicine with more patients to benefit from cancer treatments. Supported by the POSTECH Medical Device Innovation Center, the Graduate School of Artificial Intelligence, and ImmunoBiome Inc, this study was recently published in Nature Communications, an international peer-reviewed journal.
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Researchers have uncovered how post-viral fatigue syndromes, including Long COVID, become life-changing diseases and why patients suffer frequent relapses.
Arising commonly from a viral infection, Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS), is known to cause brain-centred symptoms of neuroinflammation, loss of homeostasis, brain fog, lack of refreshing sleep, and poor response to even small stresses.
Long-COVID has similar effects on people and is believed to also be caused by neuroinflammation.
Lead author Emeritus Professor Warren Tate, of the University of Otago’s Department of Biochemistry, says how these debilitating brain effects develop is poorly understood.
In a study published in Frontiers in Neurology, he and colleagues from Otago, Victoria University of Wellington and University of Technology Sydney, developed a unifying model to explain how the brain-centred symptoms of these diseases are sustained through a brain-body connection.
They propose that, following an initial viral infection or stressor event, the subsequent systemic pathology moves to the brain vianeurovascular pathways or through a dysfunctional blood-brain barrier. This results in chronic neuroinflammation, leading to a sustained illness with chronic relapse recovery cycles.