Participants in the survey were interviewed in their homes, and also visited a mobile examination center, where they recalled their food intake, received cardiometabolic health assessments, and had blood collected. That having been said, much takeout food contains ingredients that are not necessarily heart-healthy, as Jayne Morgan, MD, cardiologist and Vice President of Medical Affairs for Hello Heart, who was not involved in the study, explained: “Restaurants often reuse oils leading to oxidized fats that directly damage arteries and accelerate plaque formation,” along with refined carbohydrates and added sugars leading to insulin resistance. Then, finally,” Morgan listed, “ultra-processed ingredients that also lead to chronic inflammation. Emulsifiers, preservatives, artificial flavor enhancers, disruption of the gut microbiome, and low-fiber content.” Takeout food also frequently involves oversized portion sizes that contribute to weight gain and blood pressure increases. Michelle Routhenstein, MS, RD, CDCES, CDN, Preventive Cardiology Dietitian at Entirely Nourished, also not involved in this study, noted: “It is also important to recognize that frequent takeout use often reflects broader lifestyle pressures such as demanding schedules, limited access to cooking resources, irregular meals, and disrupted sleep, all of which can quietly compound cardiovascular risk.” “The focus can be on making small, manageable adjustments rather than complete avoidance,” she suggested. Takeout meals can also be augmented, she said, with “more anti-inflammatory, heart healthy foods such as leafy greens, colorful fruits and vegetables, nuts, seeds, legumes, whole grains, and omega-3 rich fish [that] can further support cardiovascular health.” “Even small changes can make a meaningful difference, and progress is more important than perfection,” said Routhenstein. “Well-studied cardioprotective approaches such as the Mediterranean, DASH, and plant-forward portfolio-style patterns can help people move away from a takeout-heavy menu without requiring a complete lifestyle overhaul,” said Routhenstein. “These approaches focus on adding more vegetables, fruits, legumes, whole grains, nuts, seeds, and healthy fats in a flexible, sustainable way,” she explained. “Importantly,” Routhenstein concluded, “[home-cooked menus] can be adapted to real life by simplifying meals, using convenient staples like frozen produce or canned beans and fish, and even balancing takeout choices more thoughtfully rather than eliminating them.” Researchers say a pro-inflammatory diet, which includes items such as red meat, refined carbohydrates, and sugar-sweetened beverages, is linked to a… Researchers found that consuming foods rich in polyphenols — such as coffee, berries, cocoa, and olive oil — may help improve heart health long-term. A new study suggests that consuming plant-based ultra-processed foods may lead to increased risks of cardiovascular disease and early death. Drinking orange juice can help support health by reducing inflammation and hypertension, among other factors, a recent study suggests.

New research from Fujita Health University reveals that talking can subtly delay the eyes' ability to detect and stabilize on visual information. Because driving depends heavily on fast gaze shifts, these delays may impair hazard detection and slow physical responses. Talking while driving is widely recognized as a major source of distraction, but the specific ways conversation interferes with the earliest stages of visual processing have remained largely unclear. While previous research has shown that cognitive distraction can slow braking or reduce situational awareness, the question of whether talking disrupts the foundational gaze processes that precede physical reactions has remained unanswered. Now, researchers from Fujita Health University have demonstrated that talking imposes cognitive load strong enough to delay essential eye-movement responses, potentially affecting the fast visual assessments required for safe driving. A study led by Associate Professor Shintaro Uehara and the team, including Mr. Takuya Suzuki and Professor Takaji Suzuki, published online on October 6, 2025, in PLOS ONE, examined how talking alters the temporal dynamics of gaze behavior. Any delay in initiating or completing eye movements can cascade into slower recognition of hazards, reduced accuracy of visual scanning, and delayed motor responses. "We investigated whether the impact of talking-related cognitive load on gaze behavior varies depending on the direction of eye movement," explains Dr. Uehara. To investigate this, the researchers asked 30 healthy adults to perform rapid center-out eye-movement tasks under three different conditions: talking, listening, and a no-task control. Participants were instructed to look as quickly and accurately as possible toward a peripheral visual target presented in one of eight directions. In the talking condition, participants answered general knowledge and episodic questions adapted from the Wechsler Adult Intelligence Scale and additional custom prompts. The order of conditions was randomized across three separate days. None of these effects were observed during listening or control conditions, suggesting that the act of talking and the cognitive effort required to search for and produce verbal answers create meaningful interference with gaze control mechanisms. These delays appear small in isolation, but during driving, they may accumulate into slower detection of hazards and delayed initiation of physical responses. Even hands-free conversations may introduce a cognitive load strong enough to interfere with the neural processes that initiate and guide eye movements. Because drivers often need to look downward toward pedestrians, debris, or objects on the road, these delays highlight the broad risks of conversation during visually demanding driving scenarios. Driving performance is influenced by multiple cognitive and perceptual factors, including inattentional blindness, divided attention, and the broader interference that occurs when the brain is forced to manage two demanding tasks at once. Even so, the study demonstrates that talking introduces delays at the earliest stage of visual processing before recognition, decision-making, or physical action, which means it may quietly undermine driving performance in ways that are not immediately obvious to drivers themselves. "These results indicate that the cognitive demands associated with talking interfere with the neural mechanisms responsible for initiating and controlling eye movements, which represent the critical first stage of visuomotor processing during driving," concludes Dr. Uehara. By understanding that the cognitive effort involved in conversation can degrade gaze accuracy and timing, drivers may become more mindful about when and how they choose to talk while driving. Over time, this knowledge could support safer driving behaviors, inform driver-training frameworks, inspire improvements in vehicle interface design, and guide policymakers in shaping future recommendations around cognitive distraction. Talking-associated cognitive loads degrade the quality of gaze behavior. GLP-1 agonists are pivotal in obesity care, promoting weight loss and addressing related health issues, with a focus on personalized, holistic treatment. Guillaume Bentzinger, Luis Carrillo, Philippe Robin, and Alejandro Bara-Estaún News-Medical.Net provides this medical information service in accordance with these terms and conditions. Please note that medical information found on this website is designed to support, not to replace the relationship between patient and physician/doctor and the medical advice they may provide. Hi, I'm Azthena, you can trust me to find commercial scientific answers from News-Medical.net. Registered members can chat with Azthena, request quotations, download pdf's, brochures and subscribe to our related newsletter content. A few things you need to know before we start. While we only use edited and approved content for Azthena answers, it may on occasions provide incorrect responses. Please confirm any data provided with the related suppliers or authors. Your questions, but not your email details will be shared with OpenAI and retained for 30 days in accordance with their privacy principles. Please do not ask questions that use sensitive or confidential information.

Calcium (Ca2+) drives many cellular functions, though the way it controls quality of proteins in the endoplasmic reticulum (ER), a cellular organelle that synthesizes and transports proteins, is widely unknown. This control system of protein quality, known as proteostasis, was put under a microscope by researchers to find a more thorough understanding of the process, potentially revealing clues about how to prevent Type 2 diabetes, Alzheimer's and amyotrophic lateral sclerosis (ALS). The team consisted of researchers across multiple disciplines, lead by Distinguished Associate Professor Masaki Okumura of the Tohoku University Frontier Research Institute for Interdisciplinary Sciences (FRIS) and Graduate School of Life Sciences, in an international collaborative study involving 17 research teams from Japan, Korea, and the UK. Results were published in Nature Cell Biology on November 11, 2025. With the goal of elucidating Ca2+ driven proteostasis in the ER in mind, they found that Ca2+ can induce a phase separation in PDIA6, a gene that codes for a specific, ER-localized protein responsible for protein folding and function. Therefore, if this protein loses its function, misfolding can occur. The consequences for improperly folded proteins can be dire - such as diabetes. However, not all is lost if there are mistakes in protein folding. They found that a process called calcium-driven phase separation in the ER essentially creates liquid-like droplets through condensation that can make corrections to proinsulin. Proinsulin is the insulin precursor, and too much of it can indicate a risk for Type 2 diabetes. To keep everything running smoothly, we need these condensation-like droplets to ensure proinsulin is properly folded - as opposed to forming large, aggregate clumps that can disrupt the normal pathways and cause negative health outcomes." This knowledge meaningfully contributes to our understanding of other calcium-driven processes within cells. In addition, this research could potentially be used in drug development for difficult-to-cure diseases like ALS, Alzheimer's and Type 2 diabetes. GLP-1 agonists are pivotal in obesity care, promoting weight loss and addressing related health issues, with a focus on personalized, holistic treatment. Guillaume Bentzinger, Luis Carrillo, Philippe Robin, and Alejandro Bara-Estaún News-Medical.Net provides this medical information service in accordance with these terms and conditions. Please note that medical information found on this website is designed to support, not to replace the relationship between patient and physician/doctor and the medical advice they may provide. Hi, I'm Azthena, you can trust me to find commercial scientific answers from News-Medical.net. Registered members can chat with Azthena, request quotations, download pdf's, brochures and subscribe to our related newsletter content. A few things you need to know before we start. While we only use edited and approved content for Azthena answers, it may on occasions provide incorrect responses. Please confirm any data provided with the related suppliers or authors. Your questions, but not your email details will be shared with OpenAI and retained for 30 days in accordance with their privacy principles. Please do not ask questions that use sensitive or confidential information.

A new study published today in Science Translational Medicine by researchers at The University of Texas MD Anderson Cancer Center details a therapeutic vulnerability in patients with an aggressive subtype of triple-negative breast cancer. Led by Khandan Keyomarsi, Ph.D., professor of Experimental Radiation Oncology, the study shows that simultaneous inhibition of ATR and PKMYT1 triggers a type of cell death in Rb1deficient breast cancer models. Using genomic profiling, proteomics and patient-derived xenografts, the researchers found that loss of Rb1 – a gene important for normal cell division – disrupts DNA repair processes and forces tumor cells to rely on ATR and PKMYT1 dependent pathways for survival, creating a vulnerability that can be selectively targeted. But that same deficiency makes them vulnerable to ATR and PKMYT1 inhibition. We can now identify patients who may benefit from an entirely different therapeutic strategy." What is the major finding of this study on ATR and PKMYT1 co-inhibition? The study demonstrates that simultaneously inhibiting ATR and PKMYT1 – two proteins required for maintaining genomic stability during cell division – induces cell death in Rb1-deficient breast cancers. By blocking both repair pathways, the treatment overwhelms the cancer cell's ability to correct DNA errors, leading to catastrophic DNA damage, apoptosis, tumor shrinkage and improved survival in preclinical models. How does Rb1 deficiency create a vulnerability if it also indicates resistance? Rb1 normally prevents uncontrolled cell division and helps maintain genomic integrity. When Rb1 is lost, cells accumulate DNA errors more rapidly and become prone to malignant transformation. These tumors also resist CDK4/6 inhibitors because the therapy depends on an intact Rb1 pathway to halt the cell cycle. While DNA mutations can lead to cancer development, cancer cells also need to replicate, and if they build too many mutations as they replicate, they can no longer function. By inhibiting ATR and PKMYT1 – two proteins that are also important for repairing mutations in DNA – this strategy causes and overload of mutations, leading to cell death and ultimately tumor shrinkage. Several ATR and PKMYT1 inhibitors already are in clinical trials and have received fast-track designation from the FDA. The Phase I MYTHIC Trial, which is also being led by MD Anderson researchers, is one example of a trial already testing the combination for certain mutations in solid tumors. The current findings could directly inform the development of Rb1-based biomarker strategies to identify patients most likely to benefit from dual ATR/PKMYT1 inhibition. "Beyond this combination strategy, our study also shows that Rb1 deficiency predicts sensitivity to other DNA-damaging therapies, such as chemotherapy and radiation," Keyomarsi said. "Incorporating Rb1 status into clinical decision-making could help tailor more effective, personalized treatment plans for these patients." GLP-1 agonists are pivotal in obesity care, promoting weight loss and addressing related health issues, with a focus on personalized, holistic treatment. Guillaume Bentzinger, Luis Carrillo, Philippe Robin, and Alejandro Bara-Estaún Discover how AI, flow chemistry, and NMR come together in the PiPAC project to revolutionize scalable and autonomous API production. News-Medical.Net provides this medical information service in accordance with these terms and conditions. Please note that medical information found on this website is designed to support, not to replace the relationship between patient and physician/doctor and the medical advice they may provide. Hi, I'm Azthena, you can trust me to find commercial scientific answers from News-Medical.net. Registered members can chat with Azthena, request quotations, download pdf's, brochures and subscribe to our related newsletter content. A few things you need to know before we start. Please check the box above to proceed. While we only use edited and approved content for Azthena answers, it may on occasions provide incorrect responses. Please confirm any data provided with the related suppliers or authors. Your questions, but not your email details will be shared with OpenAI and retained for 30 days in accordance with their privacy principles. Please do not ask questions that use sensitive or confidential information.

Prescription stimulants, such as Ritalin and Adderall, are widely used to treat attention deficit hyperactivity disorder (ADHD), including in children. In the U.S., about 3.5 million kids ages 3 to 17 take an ADHD medication, a number that has increased as more children have been diagnosed with the neurodevelopmental disorder. Stimulant medications have long been thought to treat ADHD by acting upon regions of the brain that control attention, but a new study by researchers at Washington University School of Medicine in St. Louis casts doubt on that thinking. Led by Benjamin Kay, MD, PhD, an assistant professor of neurology, and Nico U. Dosenbach, MD, PhD, the David M. & Tracy S. Holtzman Professor of Neurology, it shows for the first time that these drugs act primarily on the brain's reward and wakefulness centers, rather than on its attention circuitry. The findings, published Dec. 24 in Cell, suggest that prescription stimulants enhance performance by making individuals with ADHD more alert and interested in tasks, rather than directly improving their ability to focus. "I prescribe a lot of stimulants as a child neurologist, and I've always been taught that they facilitate attention systems to give people more voluntary control over what they pay attention to," said Kay, who treats patients at St. Louis Children's Hospital. Rather, the improvement we observe in attention is a secondary effect of a child being more alert and finding a task more rewarding, which naturally helps them pay more attention to it." Kay said the findings point to the importance of addressing inadequate sleep in addition to considering stimulant medication for children being evaluated for ADHD. To understand how stimulant medications affect the brain, the research team examined resting-state functional MRI, or fMRI, data - a type of neuroimaging that indicates a person's brain activity when they are not engaged in any specific task - from 5,795 children ages 8 to 11 who participated in the Adolescent Brain Cognitive Development (ABCD) Study. The researchers analyzed fMRI scans and compared brain connectivity patterns between children who took prescription stimulants and children who did not on the day of their scan. Compared with kids not taking stimulants, children who took stimulants the day of the scan showed increased activity in regions of the brain related to arousal or wakefulness and regions predicting how rewarding an activity will be. Their scans did not show significantly increased activity in regions classically associated with attention. The researchers validated their observation in an experiment on five healthy adults without ADHD who normally did not take stimulant medication. The participants were scanned using resting-state fMRI before and after taking a dose of stimulant medication, allowing for precise measurement of changes in brain connectivity. Nico U. Dosenbach, MD, PhD, the David M. & Tracy S. Holtzman Professor of Neurology In other words, the study findings suggest that rather than "lighting up" the attention centers of a child with ADHD, stimulant drugs work by helping make activities that the child normally struggles to focus on feel relatively more rewarding, he noted. "These results also provide a potential explanation for how stimulants treat hyperactivity, which previously seemed paradoxical," Dosenbach added. Compared with children with ADHD who did not take a stimulant, children with ADHD who took a stimulant medication had better grades in school (as reported by their parents) and performed better on cognitive tests given as part of the ABCD study. Despite their significant effects on brain activity, the researchers found that stimulant medications were not associated with cognitive gains in all children taking them. Children who got less than the recommended nine or more hours of sleep per night and took a stimulant received better grades in school than did kids who got insufficient sleep and did not take a stimulant. However, stimulants did not correspond with improved performance for neurotypical kids who got sufficient sleep. (It is not clear why these kids were taking stimulant medications.) "We saw that if a participant didn't sleep enough, but they took a stimulant, the brain signature of insufficient sleep was erased, as were the associated behavioral and cognitive decrements," Dosenbach said. The authors noted that this boost in performance despite a lack of sleep might carry long-term costs. He noted that children who are overtired may exhibit classic symptoms of ADHD, such as difficulty paying attention in class or declining grades, leading to a misdiagnosis in some cases when the real culprit is sleep deprivation. The stimulant medication may then appear to help by mimicking some of the effects of a good night's sleep, while still leaving the child vulnerable to long-term effects of sleep deprivation. Dosenbach and Kay's results point to the need for future studies on the potential long-term effects of stimulants on brain function. The researchers noted that these medications could have a restorative effect by activating the brain's waste clearing system during wakefulness, but it's equally likely they might cause lasting damage if used to cover up chronic sleep deficits. Kay BP, Wheelock MD, Siegel JS, Raut R, Chauvin RJ, Metoki A, Rajesh A, Eck A, Pollaro J, Wang A, Suljic V, Adeyemo B, Baden NJ, Scheidter KM, Monk JS, Whiting FI, Ramirez-Perez N, Krimmel SR, Shinohara RT, Tervo-Clemmens B, Hermosillo RJM, Nelson SM, Hendrickson TJ, Madison T, Moore LA, Miranda-Domínguez O, Randolph A, Feczko E, Roland JL, Nicol GE, Laumann TO, Marek S, Gordon EM, Raichle ME, Barch DM, Fair DA, and Dosenbach NUF. Stimulant medications affect arousal and reward, not attention networks. This work was supported by NIH grants NS140256 (EMG, NUFD), EB029343 (MW), MH121518 (SM), MH129493 (DMB), NS123345 (BPK), NS098482 (BPK), DA041148 (DAF), DA04112 (DAF), MH115357 (DAF), MH096773 (DAF and NUFD), MH122066 (EMG, DAF, and NUFD), MH121276 (EMG, DAF, and NUFD), MH124567 (EMG, DAF, and NUFD), and NS129521 (EMG, DAF, and NUFD); by the National Spasmodic Dysphonia Association (EMG); by Mallinckrodt Institute of Radiology pilot funding (EMG); by the Andrew Mellon Predoctoral Fellowship from the Dietrich School of Arts & Sciences, University of Pittsburgh (BTC); and by the Extreme Science and Engineering Discovery Environment (XSEDE) Bridges at the Pittsburgh Supercomputing Center through allocation TG-IBN200009 (BTC). The RCIF has received funding from NIH S10 program grants: 1S10OD025200-01A1 and 1S10OD030477-01. Stimulant medications affect arousal and reward, not attention networks. GLP-1 agonists are pivotal in obesity care, promoting weight loss and addressing related health issues, with a focus on personalized, holistic treatment. Guillaume Bentzinger, Luis Carrillo, Philippe Robin, and Alejandro Bara-Estaún News-Medical.Net provides this medical information service in accordance with these terms and conditions. Please note that medical information found on this website is designed to support, not to replace the relationship between patient and physician/doctor and the medical advice they may provide. Hi, I'm Azthena, you can trust me to find commercial scientific answers from News-Medical.net. Registered members can chat with Azthena, request quotations, download pdf's, brochures and subscribe to our related newsletter content. A few things you need to know before we start. While we only use edited and approved content for Azthena answers, it may on occasions provide incorrect responses. Please confirm any data provided with the related suppliers or authors. Your questions, but not your email details will be shared with OpenAI and retained for 30 days in accordance with their privacy principles. Please do not ask questions that use sensitive or confidential information.