A citizen-science collaboration in New York has turned up a half-dozen birds infected with the avian flu virus.New Yorkers, beware: If you come across a bird or animal that is sick, dead or behaving strangely, keep yourself and your pets at a safe distance. The bird flu virus, H5N1, is present in at least some small fraction of New York City birds, according to a new study.The finding is not entirely surprising, given that H5N1 has now been shown to affect migratory birds, a wide range of wild animals, poultry and, as of last month, dairy cows. Still, its discovery in the city is an unpleasant reminder that urban spaces are not exempt.People generally associate zoonotic diseases with rural settings, farms or the wilderness, said Florian Krammer, a flu expert at the Icahn School of Medicine at Mount Sinai in New York who led the study, which was published online last week.But New York City has many green spaces and bodies of water used by migratory and local birds, he said: “There is an extensive interface between wild animals and humans in cities.”“There is no reason to panic, but it’s good to be aware of it,” he added.Last week, the Centers for Disease Control and Prevention warned health care providers to watch for signs of bird flu infection. So far, only two Americans have been reported as infected with H5N1, one in 2022 and the other earlier this month.The virus has caused large outbreaks in mink and foxes, and wiped out thousands of marine mammals, especially in South America. Scientists have tracked the virus along migratory routes and stopovers, among wild birds in rural areas and commercial poultry operations and, most recently, among cattle on dairy farms.We are having trouble retrieving the article content.Please enable JavaScript in your browser settings.Thank you for your patience while we verify access. If you are in Reader mode please exit and log into your Times account, or subscribe for all of The Times.Thank you for your patience while we verify access.Already a subscriber? Log in.Want all of The Times? Subscribe.

Fifteen words are roiling the global alcohol industry.Beginning in 2026, containers of beer, wine and liquor sold in Ireland will be required by law to bear a label in red capital letters with two warnings: “THERE IS A DIRECT LINK BETWEEN ALCOHOL AND FATAL CANCERS” and “DRINKING ALCOHOL CAUSES LIVER DISEASE.”The requirement, signed into law last year, is backed by decades of scientific research and goes much further than any country has thus far communicated the health risks of alcohol consumption. It has sparked fierce opposition from alcohol businesses worldwide, but it is also inspiring a push in some other countries to pursue similar measures.“It’s an important step,” said Dr. Timothy Naimi, the director of the Canadian Institute for Substance Use Research at the University of Victoria. “People who drink should have the right to know basic information about alcohol, just as they do for other food and beverage products.”In Thailand, the government is in the final stages of drafting a regulation requiring alcohol products to carry graphic images accompanied by text warnings such as “alcoholic beverages can cause cancer,” according to The Bangkok Post.A bill has been introduced in the Canadian Parliament that would require labels on all alcoholic beverages to communicate a “direct causal link between alcohol consumption and the development of fatal cancers.”Last week, the Alaska State Legislature held a committee hearing on a bill that would require businesses selling alcohol to post signs carrying a cancer warning.We are having trouble retrieving the article content.Please enable JavaScript in your browser settings.Thank you for your patience while we verify access. If you are in Reader mode please exit and log into your Times account, or subscribe for all of The Times.Thank you for your patience while we verify access.Already a subscriber? Log in.Want all of The Times? Subscribe.

Brain organoids, though often referred to as “mini brains,” are not truly human brains. But the concerns over these lab-grown brain tissues, especially when they are developed from human fetal tissues, can be very human indeed.
Researchers from the Graduate School of Humanities and Social Sciences at Hiroshima University offer valuable insights into the complexities inherent in brain organoid research, making significant contributions to the ongoing discourse surrounding this innovative biotechnology and paving the way for informed decision-making and legal and ethical stewardship in the pursuit of scientific advancement.
Their paper was published on March 4 in EMBO Reports.
Brain organoids are three-dimensional human brain tissues derived from stem cells, which are capable of developing into many different cell types. They replicate the complexity of the human brain in a laboratory setting, allowing researchers to study brain development and diseases in the hopes of acquiring vital insights and making innovative medical advancements.
Traditionally, brain organoids are grown from pluripotent stem cells, an especially potent sub-type that is typical of early embryonic development, but new technologies now make it possible to generate these organoids from human fetal brain cells. This method comes, however, with even more heated legal and ethical debates about brain organoids — debates that are already intense in conventional organoid research.
“Our research seeks to illuminate previously often-overlooked ethical dilemmas and legal complexities that arise at the intersection of advanced organoid research and the use of fetal tissue, which is predominantly obtained through elective abortions,” said Tsutomu Sawai, an associate professor at Hiroshima University and lead author of the study.
The study highlights the urgent need for a sophisticated and globally harmonized regulatory framework tailored to navigate the complex ethical and legal landscape of fetal brain organoid (FeBO) research. The paper emphasizes the importance of informed consent protocols, ethical considerations surrounding organoid consciousness, transplantation of organoids into animals, integration with computational systems, and broader debates related to embryo research and the ethics of abortion.
“Our plan is to vigorously advocate for the development of thorough ethical and regulatory frameworks for brain organoid research, including FeBO research, at both national and international levels,” said Masanori Kataoka, a fellow researcher at Hiroshima University.
“Rather than being limited to issues of consciousness, it’s imperative, now more than ever, to systematically advance the ethical and regulatory discussion in order to responsibly and ethically advance scientific and medical progress,” Sawai said.
Moving forward, the research duo plans to continue supporting the advancement of ethical and regulatory discussions surrounding brain organoid research. By promoting responsible and ethical progress in science and medicine, they aim to ensure that all research involving brain organoids, including FeBOs, is conducted within a framework that prioritizes human dignity and ethical integrity.

Coronary artery disease and major depression may be genetically linked via inflammatory pathways to an increased risk for cardiomyopathy, a degenerative heart muscle disease, researchers at Vanderbilt University Medical Center and Massachusetts General Hospital have found.
Their report, published April 5 in the journal Nature Mental Health, suggests that drugs prescribed for coronary artery disease and depression, when used in combination, potentially may reduce inflammation and prevent the development of cardiomyopathy.
“This work suggests that chronic low-level inflammation may be a significant contributor to both depression and cardiovascular disease,” said the paper’s corresponding author, Lea Davis, PhD, associate professor of Medicine in the Division of Genetic Medicine and Vanderbilt Genetics Institute.
The connection between depression and other serious health conditions is well known. As many as 44% of patients with coronary artery disease (CAD), the most common form of cardiovascular disease, also have a diagnosis of major depression. Yet the biological relationship between the two conditions remains poorly understood.
A possible connection is inflammation. Changes in the levels of inflammatory markers have been observed in both conditions, suggesting that there may be a common biological pathway linking neuroinflammation in depression with atherosclerotic inflammation in CAD.
In the current study, the researchers used a technique called transcriptome-wide association scans to map single nucleotide polymorphisms (genetic variations) involved in regulating the expression of genes associated with both CAD and depression.
The technique identified 185 genes that were significantly associated with both depression and CAD, and which were “enriched” for biological roles in inflammation and cardiomyopathy. This suggests that predisposition to both depression and CAD, which the researchers called (major) depressive CAD, or (m)dCAD, may further predispose individuals to cardiomyopathy.

However, when the researchers scanned large electronic health record databases at VUMC, Mass General, and the National Institutes of Health’s All of Us Research Program, they found the actual incidence of cardiomyopathy in patients with the enriched genes for (m)dCAD was lower than in patients with CAD alone.
One possible explanation is that medications prescribed for CAD and depression, such as statins and antidepressants, may prevent development of cardiomyopathy by reducing inflammation, the researchers concluded.
“More research is needed to investigate optimal treatment mechanisms,” Davis added, “but at a minimum this work suggests that patient heart and brain health should be considered together when developing management plans to treat depression or cardiovascular disease.”
Kritika Singh, PhD, the paper’s first author, is a former graduate student in the Davis lab who is now a postdoctoral Innovation Fellow at Novartis in Cambridge, Massachusetts.
Other VUMC co-authors are Tyne Miller-Fleming, PhD, Peter Straub, MS, Nancy Cox, PhD, founding director of the Vanderbilt Genetics Institute, and institute members Quinn Wells, MD, PharmD, MSCI, associate professor of Medicine in the Division of the Cardiovascular Medicine, and Emily Hodges, PhD, assistant professor of Biochemistry.
The research was supported by National Institutes of Health grants R56MH120736, R01H118233, 1F31MH124306, and 1R01HL140074, and an American Heart Association Fellowship.

In a recent study, researchers at Huntsman Cancer Institute at the University of Utah (the U) found a surprising trend in families with male infertility: an increased risk of certain cancers. This discovery could lead to a more personalized approach to cancer risk assessments, making cancer prevention more effective.
According to the National Institutes of Health, around 9% of men at reproductive age have experienced fertility problems.
“We know that men who experience infertility tend to have more health issues like cardiovascular disease, autoimmune conditions, earlier mortality, chronic health conditions, and cancer,” says Joemy Ramsay, PhD, the study’s lead investigator, researcher at Huntsman Cancer Institute, and assistant professor in the Division of Urology at the U. “We wanted to look at whether the family members of these men were at higher risk for these conditions.”
Ramsay has a background in public health, specializing in occupational and environmental exposure. This study represents the first step in determining family members’ correlated risk levels to diseases, such as cancer. Ramsay explains that since family members share similar genetic factors, environments, and lifestyles, it would be easier to identify other things impacting their cancer risk. Once general risk has been assessed, etiological factors can be more accurately evaluated in determining the part they play in a diagnosis.
Using the Utah Population Database, one of the world’s richest sources of genetic and public health information, Ramsay and her team, which included Heidi Hanson, MS, PhD, Nicola Camp, PhD, and Myke Madsen, looked at parents, siblings, children, and even aunts, uncles, and cousins, of men who have been diagnosed with infertility.
By observing several types of cancer at once, the team was able to develop an algorithm that clusters similar things together. This algorithm made it possible to identify roughly 13 characteristic patterns. The patterns were based on families possessing similar multi-cancer risks, instead of looking at only one cancer type at a time.
“Both cancer and subfertility are complex diseases and processes,” says Ramsay. “This method helps create similar family groups, making it easier to uncover the reason behind a family being at high risk for certain diseases over others.”
For families with male infertility, these findings may prompt additional conversations with their doctors.

“While the link is still not fully understood, it is important to have these conversations with our families, and bring your concerns to your medical team,” says Ramsay.
Further research is needed to continue to establish a link between male infertility and cancer risk. Understanding the reason behind a risk may ultimately lead to more personalized courses of treatment, screening, and prevention.
Huntsman Cancer Institute leads the way in educating patients on how to prevent and treat cancer. For more information on genetic testing, visit our Family Cancer Assessment Clinic.
This study was supported by the National Institutes of Health/National Cancer Institute including P30 CA042014 and Huntsman Cancer Foundation. The chatbots were developed in a recently completed trial funded by the Inherited Cancer Syndrome Collaborative of the Cancer Moonshot initiative.

In findings published in Cell Reports, senior author Jerold Chun, M.D., Ph.D., and team also discovered that the biological instructions within these vesicles differed significantly in postmortem brain samples donated from patients suffering from Alzheimer’s disease.
Researchers call the tiny brain bubbles under scrutiny in this study small extracellular vesicles (sEVs). These tiny biological water balloons are produced by most cells in the body to ferry a wide variety of proteins, lipids and byproducts of cellular metabolism, as well as RNA nucleic acid codes used by recipient cells to construct new proteins.
Because this biologically active cargo can easily elicit changes in other cells, scientists are interested in brain sEVs as a medium for passing along normal as well as bungled instructions for misfolded proteins that accumulate in the brain as neurodegenerative diseases such as Alzheimer’s disease progress.
To be a potential contributor to the buildup of unwanted proteins, sEVs would have to carry blueprints with sufficient information to enable other cells to produce the problematic proteins. Most previous research had indicated that the messenger RNA (mRNA) carrying plans for proteins were chopped into too many shorter fragments to allow recipient cells to change their construction patterns.
“We found quite the opposite to be true in our study,” says Chun, professor in the Center for Genetic Disorders and Aging Research at Sanford Burnham Prebys. “We identified more than 10,000 full-length mRNAs through the use of a relatively newer DNA sequencing technique called PacBio long-read sequencing.”
The team isolated sEVs from the prefrontal cortex of 12 postmortem brain samples donated from patients diagnosed with Alzheimer’s disease and 12 from donors without Alzheimer’s disease (or any other known neurological disease). Nearly 80% of identified mRNAs were full-length, allowing them to be transcribed by recipient cells into viable proteins.
“To corroborate the results of long-read sequencing in the human samples, we also looked at vesicles isolated from mouse cells,” says first author Linnea Ransom, Ph.D., postdoctoral fellow at Sanford Burnham Prebys. “We found similar averages of between 78% and 86% full-length transcripts in three brain cell types: astrocytes, microglia and neurons.”
In addition to analyzing and validating the results regarding the length of mRNAs in brain sEVs, the researchers compared the sequence of genes reflected in the sEV mRNA transcriptome. In Alzheimer’s disease samples, 700 genes showed increased expression whereas nearly 1500 were found to have reduced activity.

The scientists determined that the 700 upregulated genes are associated with inflammation and immune system activation, which fits within known patterns of brain inflammation present in neurodegenerative diseases such as Alzheimer’s disease. The researchers also found many genes associated with Alzheimer’s disease in prior genome-wide association studies also were present in Alzheimer’s disease sEVs.
“The changes in gene expression contained in these vesicles reveal an inflammatory signature that may serve as a window into disease processes occurring in the brain as Alzheimer’s disease progresses,” says Chun.
Following this study, Chun and team will dig deeper into how cells package sEVs and how the enclosed mRNA codes lead to functional changes in other brain cells affected in Alzheimer’s disease. Better understanding of sEVs and their mRNA contents may enable the discovery of biomarkers that could be used to improve early detection of Alzheimer’s disease and potentially other neurological conditions, while identifying new disease mechanisms to provide new therapeutic targets.
“Additionally, sEVs naturally occur as a vehicle for transporting biologically active cargo between cells, so it also may be possible to leverage them as a targeted delivery system for future brain therapies” says Chun.
Additional authors on the study include Linnea S. Ransom, Christine S. Liu, Emily Dunsmore, Carter R. Palmer, Juliet Nicodemus, Derya Ziomek and Nyssa Williams, all at Sanford Burnham Prebys.
The study was supported by the National Institute on Aging (R01AG065541 and R01AG071465), National Institute of General Medical Sciences (T32GM007752) and Rotary International.

For heart attack patients, treating only the coronary artery that caused the infarction works just as well as preventive balloon dilation of the other coronary arteries, according to a new large study by researchers at Karolinska Institutet and others. The results are published in the New England Journal of Medicine.
Heart attack is a common disease with risks of serious complications. It has long been unclear what the best strategy is for treating narrowings in coronary arteries separate from the specific vessel that caused the infarction.
A new large Swedish study has investigated whether it is sufficient to treat only the coronary artery that caused the infarction, or whether long-term results are better if other narrowed vessels are also treated with balloon dilation as a preventive measure.
The clinical randomized study included 1542 patients from 32 hospitals in 7 countries. In the Swedish part, the SWEDEHEART registry was used to conduct the randomization and collect data. Patients were followed up for five years after the procedure.
The results show no difference between the groups in terms of new heart attacks, new unplanned balloon dilations or the total number of all-cause deaths.
“This is somewhat surprising. Our hypothesis was that it would be beneficial to do preventive angioplasty,” says Felix Böhm, a senior physician at the Department of Clinical Sciences, Danderyd Hospital at Karolinska Institutet, who led the study.
However, when it comes to problems with angina, the study shows that it is possible to avoid patients coming back for new balloon dilations through preventive treatment. According to Felix Böhm, this suggests that we should still aim for complete treatment of all vessels.

“But for those patients where there is some circumstance that makes a complete revascularization complicated, one might choose to wait, since there was no difference in the most serious complications — new heart attack and death,” says Felix Böhm.
If problems with angina occur, these patients can then come back later for a new treatment, according to Felix Böhm.
“A positive finding of the study was that most patients do not come back with new problems, regardless of the treatment strategy chosen. “Nowadays, heart attack patients are so well treated with drugs that it is difficult to find other interventions that provide further significant risk reduction,” says Felix Böhm.
The researchers will now go on to investigate how angina and other quality of life parameters in the patients were affected by the different treatment strategies, as well as health economic aspects of the chosen strategy.
The research was conducted by Uppsala Clinical Research Center (UCR) at Uppala University. The legal sponsor was Karolinska University Hospital. The study was funded by the Swedish Research Council, Hjärt-Lungfonden, Region Stockholm, Abbott and Boston Scientific. The companies had no influence on study design, results analysis or article writing.

Understanding heart function and disease, as well as testing new drugs for heart conditions, has long been a complex and time-consuming task. A promising way to study disease and test new drugs is to use cellular and engineered tissue models in a dish, but existing methods to study heart cell contraction and calcium handling require a good deal of manual work, are prone to errors, and need expensive specialized equipment. There clearly is a critical medical need for a more efficient, accurate, and accessible way to study heart function, using a methodology based on artificial intelligence (AI) and machine learning.
BeatProfiler, new tool to rapidly analyze heart cell function
Researchers at Columbia Engineering unveiled a groundbreaking new tool today that addresses these challenges head-on. BeatProfiler is a comprehensive software that automates the analysis of heart cell function from video data and is the first system to integrate the analysis of different heart function indicators, such as contractility, calcium handling, and force output into one tool, speeding up the process significantly and reducing the chance for errors. BeatProfiler enabled the researchers to not only distinguish between different diseases and levels of their severity but also to rapidly and objectively test drugs that affect heart function. The study was published on April 8 in IEEE Open Journal of Engineering in Medicine and Biology.
“This is truly a transformative tool,” said project leader Gordana Vunjak-Novakovic, University Professor and the Mikati Foundation Professor of Biomedical Engineering, Medical Sciences, and Dental Medicine at Columbia. “It’s fast, comprehensive, automated, and compatible with a broad range of computer platforms so it is easily accessible to investigators and clinicians.”
Software is open-source
The team, which included Barry Fine, assistant professor of medicine (in Cardiology) at Columbia University Irving Medical Center, elected not to file a patent application, and instead are offering the AI software as open source, so it can be directly used — for free — by any lab. They believe that this is important for disseminating the results of their research, as well as for getting feedback from users in academic, clinical, and commercial labs that can help the team to further refine the software.
The need to diagnose heart disease quickly and accurately
This project was driven, like much of Vunjak-Novakovic’s research, by a clinical need to diagnose heart diseases more quickly and accurately. This was a project that was several years in the making in which the team added different features piece by piece. While the overarching need was to develop a tool that could better capture the function of the cardiac models that the team was building to study cardiac diseases and assess the efficacy of potential therapeutics, the researchers had an urgent need to quickly and accurately assess the function of their cardiac models in real-time.

As the lab was making more and more cardiac tissues through innovations such as milliPillar and multiorgan tissue models, the increased capabilities of the tissues required the researchers to develop a method to more rapidly quantify the function of cardiomyocytes (heart muscle cells) and tissues to enable studies exploring genetic cardiomyopathies, cosmic radiation, immune-mediated inflammation, and drug discovery.
Collaborators in software development, machine learning, and more
In the last year and a half, lead author Youngbin Kim and his coauthors developed a graphical user interface (GUI) on top of the code so that biomedical researchers with no coding expertise could easily analyze the data with just a few clicks. This brought together experts in software development (for the GUI development), machine learning (for developing computer vision technology and disease/drug classifiers), signal processing (for processing contractile and calcium signals), engineering (translating pillar deflection on the cardiac platform to mechanical force), and user experience by lab members (to give feedback for improvements in the interface).
The results
The study showed that BeatProfiler could accurately analyze cardiomyocyte function, outperforming existing tools by being faster — up to 50 times in some cases — and more reliable. It detected subtle changes in engineered heat tissue force response that other tools might miss.
“This level of analysis speed and versatility is unprecedented in cardiac research,” said Kim, a PhD candidate in Vunjak-Novakovic’s lab at Columbia Engineering. “Using machine learning, the functional measurements analyzed by BeatProfiler helped us to distinguish between diseased and healthy heart cells with high accuracy and even to classify different cardiac drugs based on how they affect the heart.”
What’s next
The team is working to expand BeatProfiler’s capabilities for new applications in heart research, including a full spectrum of diseases that affect the pumping of the heart, and drug development. To ensure that BeatProfiler can be applied to a wide variety of research questions, they are testing and validating its performance across additional in vitro cardiac models, including different engineered heart tissue models. They are also refining their machine-learning algorithm to extend and generalize its use to a variety of heart diseases and drug effect classification. The long-term goal is to adapt BeatProfiler to pharmaceutical settings to speed up the testing of hundreds of thousands of candidate drugs at once.

Despite having an overall survival rate of 94%, B-cell acute lymphoblastic leukemia (B-ALL), the most common childhood cancer, can prove challenging to treat, with survival among relapsed or resistant cases falling between 30-50%. Recent work by St. Jude Children’s Research Hospital scientists discovered which tumor cells resist treatment and why. This enabled the rational design of a combination therapy that better controlled high-risk subtypes of B-ALL in mouse models. The findings were published today in Cancer Cell.
“We found a new explanation of B-ALL sensitivity to asparaginase, which is one of the most commonly used drugs for this disease,” said senior co-corresponding author Jun J. Yang, PhD, St. Jude Department of Pharmacy and Pharmaceutical Sciences vice-chair. “Although asparaginase has been around for almost 50 years, the way we use this drug for ALL remains imprecise. This is partly because we still do not fully understand the mechanism by which it kills leukemia cells.”
Scientists showed combining the classic drug asparaginase (a chemotherapy) with a newer drug, venetoclax (a BCL-2 targeted therapy), was most effective at treating B-ALL in laboratory models. The combination reduced the number of leukemia cells more than either drug alone and worked faster. The improved effects were consistent across three different high-risk subtypes of this cancer.
“This discovery was enabled by single-cell systems biology analysis of B cell development and integration with B-ALL drug sensitivity profiling and bulk RNA-sequencing data,” said co-corresponding author Jiyang Yu, PhD, St. Jude Department of Computational Biology interim chair. “Our single-cell network analysis revealed the protein BCL-2 as a hidden vulnerability in the asparaginase-resistant tumor developmental stage.”
“Administering asparaginase alongside venetoclax may lower the risk of ALL relapse, the major reason for treatment failure,” said co-author Ching-Hon Pui, MD, St. Jude Department of Oncology Fahad Nassar Al-Rashid Endowed Chair of Leukemia Research. “Ideally, we aim for venetoclax to potentiate the anti-leukemia properties of asparaginase while keeping its toxicity levels in check. These concepts warrant further investigation in future clinical trials.”
Venetoclax is already Food and Drug Administration-approved for use in other pediatric cancers, making it an attractive candidate. The drug has proven safe in those settings, paving the way for future approval in B-ALL treatment. The largest hurdle was understanding how venetoclax works with asparaginase to stop B-cell leukemia.
B-cell development stage is a challenge and vulnerability in B-ALL
B-ALL is a cancer derived from white blood cells called B cells. Under normal circumstances, B cells develop from immature to fully mature, passing through eight steps. In cancers, cells can get stuck in an intermediate stage of development. In a related disease, T-cell acute lymphoblastic leukemia, Yang and Yu previously found, as reported in Nature Cancer 2021, that the developmental stage where T cells get stuck determines their sensitivity to therapeutics. The researchers wanted to understand what made cells in a specific stage respond to which drug, hoping that such understanding would present new therapeutic opportunities.

“In this case, we found tumor B cells are stuck in two major stages,” Yu said. “One is an earlier stage that is more resistant to asparaginase and another later stage that is more sensitive to it.”
Yu looked at gene expression data from hundreds of thousands of individual cancerous B cells to understand what was different about them. After identifying the two dominant B-cell development stages of B-ALL, pre-pro-B (early) and pro-B (late), his lab looked for the genes upregulated in the resistant early cells to identify potential vulnerabilities to target therapeutically.
“The protein BCL-2 caught our attention, as it seems to be a driver of asparaginase-resistance in leukemia cells with pre-pro-B features,” Yu said.
B cell lymphoma protein 2 (BCL-2) is a protein involved in cell death. Cancer cells use it to evade the systems that normally cause them to self-destruct. The protein is also downstream of mTOR, the protein targeted by asparaginase. Findings showed that BCL-2 was activated in cancer cells resistant to that drug. That resistance relationship motivated the scientists to try venetoclax, which targets the protein BCL-2, in a combination approach.
“When you add asparaginase, you hit mTOR signaling,” Yang said. “In turn, that upregulates the BCL-2 activity, making the cells more sensitive to venetoclax.”
The work also has implications for other cancers because incorrect development underlies many forms of the disease. Single-cell gene sequencing and analysis may provide similar opportunities to improve therapies in those contexts.
“We showed that developmental arrest of cancer cells can make them sensitive to certain drugs,” Yang said. “Once we determine the pathways involved, we can find new drug combinations to improve treatment outcomes.”

If you had to decide whether to receive $40 in seven days or $60 in 30 days, which would you choose? Your answer could have less to do with whether you are a patient or impatient person than with how the choice is presented, according to a new paper published in Nature Communications.
The research found that first revealing the time delay — seven to 30 days — made people tend to prefer the shorter-term, “impatient” option, while first revealing the greater reward of the 30-day option encouraged people to choose the “patient” option of waiting to receive more money. The amount of time allotted to decide also influences their choices, but not always in the way you might expect. In some cases, people were more patient when they had less time to decide.
“The takeaway message is that people can be impatient or exhibit a lack of self-control for many reasons,” said corresponding author Ian Krajbich, an associate professor of psychology at UCLA. “It may in part reflect their true patience but it may also be due to attentional biases, like how prominently delay information is presented. Immediately focusing on the benefits of waiting might help people improve their self-control.”
Krajbich, who studies the cognitive process by which people make choices, and colleagues at Zhejiang University and Hangzhou Normal University, led by Fadong Chen, asked a total of 353 college student volunteers to choose between patient and impatient alternatives, for example to receive $40 in seven days or $60 in 30 days, by clicking their choice on a computer screen while software tracked and recorded the movements of their mouse. In some cases, participants had to make their decisions in two seconds, in others they had unlimited time or had to wait 10 seconds before choosing. At the end of the study, participants earned money based on one decision.
Whether the mouse shot straight to one of the options or wandered a little as the participant considered their options revealed the order in which they were considering dimensions of the task, and at what point in time their mouse movements were first influenced by either the delays or rewards.
More than half the participants patiently chose the “larger later” option regardless of time constraint: Surprisingly, when given the least time to think about it, they made the most patient decisions. With just two seconds to choose, 65% opted for the “larger later” option. With unlimited time, 59% chose the “larger later” option, as did only 54% of those who had to wait 10 seconds before choosing. But participants who generally favored the “smaller sooner” options showed the opposite pattern, tending to prefer the “larger later” option when they had more time to think about it.”If you’re somebody who focuses on the rewards first, time pressure accentuates that and makes you more patient,” Krajbich said. “And if you’re a little impatient by nature and focus on delays first, time pressure magnifies that impatience. Time pressure has different effects for different people. It enhances inherent bias.”
But the researchers found that they could manipulate that bias by changing how they presented information about the choices.

The researchers then repeated the experiments, but altered how the information was presented, sometimes revealing the delay first and sometimes revealing the rewards first. In these experiments, participants were allowed to make choices at various times, such as after seeing just one piece of information or after seeing them all.
These experiments revealed that when shown the rewards first, participants made more “larger later” choices. When the time delay was presented first, they made more “smaller sooner” choices. People were more patient when they saw rewards before delays.
Research on decision-making has shown that when people are making decisions, they have to evaluate their options over time because they often don’t immediately know what to do. Because people have limited attention, they tend to focus on one dimension of the choice at a time.
In the experiments, these two dimensions were delay or reward, and participants tended to consider the amounts first and then the delays, but this varied across people. Those who were less patient in their choices were more likely to consider the delays first.
“If people consider amounts first, they’re more likely to choose the patient option, and if they consider the delays first, they’re more likely to choose the impatient option. If you’re trying to get people to be more patient by getting them to slow down or speed up their decisions, you need to know which dimension they’re going to focus on first. That will determine the appropriate intervention,” Krajbich said.
The findings could be applied where people are being encouraged to make life choices that will benefit them in the long run, such as eating healthier, exercising or saving for retirement.
“You want to emphasize those future large rewards and try to deemphasize how long it’s going to take,” Krajbich said. “Try to have the reward information come first.”