Category: 8. Health

Discover the hottest new tools to study protein biology this August at the American Society for Biochemistry and Molecular Biology’s 15th International Symposium on Proteomics in the Life Sciences. This five-day symposium will be held August 17–21 at the Broad Institute of the Massachusetts Institute of Technology and Harvard University. Each day will be packed with scientific sessions, networking opportunities and more.

Meeting organizer Kathryn Lilley, a professor and group leader at the University of Cambridge, said she wants the symposium to give attendees a glimpse into the future of proteomics. She first attended this meeting more than a decade ago.

“Although I was in awe of all these very decorated colleagues — leaders in their field — everybody was super welcoming,” Lilley said.

The 2025 organizing committee includes Lilley; A. L. Burlingame, professor of pharmaceutical chemistry at the University of California, San Francisco; Steven Carr, senior director of proteomics at the Broad Institute; Ileana Cristea, director of graduate studies at Princeton University and ASBMB’s Molecular & Cellular Proteomics editor-in-chief; and Bernhard Küster, professor of proteomics and bioanalytics at the Technical University of Munich.

Lilley said this year’s conference will continue to foster that welcoming atmosphere while showcasing speakers with diverse expertise and offering a program that examines the proteome from all angles.

Plenary talks from leaders in their fields will explore innovative proteomic and post-translational modification analyses in cancer and precision medicine, pioneering approaches in drug discovery through targeted protein degradation, and fresh insights into virus-host interactions that shape immune and metabolic responses. Lilley hopes attendees will discover unexpected opportunities to collaborate.

“These sets of speakers don’t necessarily come together in a lot of the larger meetings in our field, so I think that itself is very interesting and very empowering,” she said. “You’ll get people who have not met but will see some sort of alignment in their research programs and their methodologies.”

In addition to plenary and session talks, organizers will select a few abstracts for short talks. Most abstract submitters will have the opportunity to present a poster.

“Everybody takes it very seriously, and every poster will get a lot of interest and a lot of traffic,” she said.

Looking ahead, the program will take a holistic view of the field and highlight emerging areas such as spatial proteomics, single-cell proteomics, multiomics, proteoforms and immunopeptidomics.

“There’s going to be an element of crystal ball gazing and future-proofing proteomics as well,” she said.

Lilley encouraged researchers new to proteomics to attend and explore how these techniques might expand and diversify their work.

“Everybody, whatever career stage they are, needs to have their horizons expanded to be able to look for new opportunities,” she said. “This meeting is a great place to do just that.”

The regular registration deadline is July 23. Register today!

An engineered protein turns off the kind of immune cells most likely to damage tissue as part of Type-1 diabetes, hepatitis, multiple sclerosis, shows a new study in mice.

In these autoimmune diseases, T cells mistakenly target the body’s own tissues instead of invading viruses or bacteria as they would during normal immune responses. Treatments focused on T cells have been elusive because blocking their action broadly weakens the immune system and creates risk for infections and cancer.

Published online June 30 in the journal Cell, the study revealed that holding closely together two protein groups (signaling complexes) on T cells, including one found more often on T cells involved autoimmune disease, shuts down those T cells in a limited way.

Led by researchers at NYU Langone Health, the Chinese Academy of Sciences, and Zhejiang University, the study built on biology newly discovered by the team to design an antibody that attached to both T cell signaling complexes, the T cell receptor and the LAG-3 checkpoint, held them closely together, and eliminated autoimmune tissue damage in three mouse models of disease.

Antibodies are proteins made by the immune system that label specific markers on cells for notice by the immune system. Researchers learned decades ago to engineer antibodies to target certain molecules as treatments, and more recently, antibodies that attach to two targets.

Our findings reveal an intricate mechanism that enables a careful treatment approach to T-cell driven autoimmune diseases, which currently lack effective immunotherapies.”

Jun Wang, PhD., co-senior study author, assistant professor, Department of Pathology at NYU Grossman School of Medicine

Held in place

The study results are based on the presence on T cells of T-cell receptors (TCRs) and checkpoints. TCRs, although shaped so that bits of invading bacteria or viruses fit into them to activate the T cell, are turned on by the body’s own proteins in autoimmune diseases. Checkpoints like LAG-3 are also turned on by specific signaling partners, but when this occurs they have the opposite effect of TCRs, suppressing the T cell’s activity.

Also important to the new study results is that TCR-triggering molecules must be presented to T cell receptors by another set of immune cells that “swallow” foreign (e.g., microbial) or bodily substances and display on their surfaces through protein groups called major histocompatibility complexes (MHC-II) just the small protein pieces that activate a given TCR.

“We discovered that, as a T cell’s surface draws close to the MHC-II presenting its TCR trigger molecule, the T cell receptor gets particularly close to LAG-3”, said co-first author Jasper Du, a third-year medical student in Dr. Wang’s lab. “For the first time, we found that this proximity is central to the ability of LAG-3 to dial back T cell activity.”

Mechanistically, the research team found that the proximity of LAG-3 lets it loosely stick to part of the T cell receptor called CD3ε (like two oily globs interacting). This attachment was found to pull on CD3ε enough to disrupt its interaction an enzyme called Lck, which is crucial for T cell activation. MHC-II can theoretically attach to LAG-3 and TCR at the same time, but not frequently enough to maximize LAG-3’s ability to dial down T cells, the researchers said.

In addition, “checkpoints” like LAG-3 are used by the immune system to turn off T cells when the right signals, given off by normal cells, dock in to avert self-attack (autoimmunity). Cancer cells put off signaling molecules that dock into checkpoints and sabotage the ability of T cells to attack them. Therapies called checkpoint inhibitors counter this effect.

LAG-3 turns off T cells, but less easily due to its spatial requirements than another checkpoint called PD-1. This feature makes LAG-3 inhibitors weaker as anti-cancer cancer treatment than PD-1-inhibiting antibody treatments that have become a mainstay, but likely better when the immune system is overactive, and targeted T cell suppression is required for maximum safe effect.

Based on their discovery of the critical role of TCR proximity in LAG-3 function, the research team designed a molecule that enforces LAG-3/TCR proximity to achieve better LAG-3-dependent TCR inhibition and suppression of T cell responses. Their “bi-specific” antibody held LAG-3 and the T cell receptor together more strongly than MHC-II, and without depending on it.

The current authors’ bispecific antibody, named the LAG-3/TCR Bispecific T cell Silencer or BiTS, potently suppressed T cell responses and lessened inflammatory damage to insulin-producing cells (insulitis) in BiTS-treated mice with a version of Type 1 diabetes. In autoimmune models of hepatitis, BiTS treatment reduced T cell infiltration and liver damage.

With the diabetes and hepatitis disease models largely driven by one type of T cells (CD8+), the team also used a mouse model of multiple sclerosis known to be driven by a second major T cell type (CD4+). The team treated mice prone to develop multiple sclerosis with short-term, preventive BiTS prior to the onset of disease symptoms, and BiTS-treated mice had reduced disease by a standard measure.

“Our study advances our understanding of LAG-3 biology and may foster more proximity-based, spatially-guided therapeutic designs like BiTS as immunotherapy for other human diseases,” said co-first author Jia You, a research scientist in Dr. Wang’s lab.

Along with Dr. Wang, corresponding authors of the study were Jack Wei Chen of the Department of Cell Biology and Department of Cardiology at the Second Affiliated Hospital Zhejiang University School of Medicine in China; as well Jizhong Lou of the State Key Laboratory of Epigenetic Regulation and Intervention, Institute of Biophysics, Chinese Academy of Sciences.

Also other authors from the NYU Grossman School of Medicine were Jia Liu, Qiao Lu, Connor James, Ryan Foster, and Eric Rao in the Department of Pathology at New York University Grossman School of Medicine; Meng-ju Lin and Catherine Pei-ju Lu in the Hansjörg Wyss Department of Plastic Surgery and Department of Cell Biology; and Michael Cammer at the Microscopy Core, Division of Advanced Research Technologies, and Shohei Koide of the Perlmutter Cancer Center. Also making important contributions were Hui Chen at the State Key Laboratory of Epigenetic Regulation and Intervention, Institute of Biophysics, Chinese Academy of Sciences, and Yong Zhang from University of Chinese Academy of Sciences; Wei Hu and Jie Gao at The Second Affiliated Hospital, Zhejiang University School of Medicine; and Weiwei Yin in the Key Laboratory for Biomedical Engineering of the Ministry of Education, College of Biomedical Engineering and Instrument Science, also at Zhejiang University.

The study was supported principally by a translational advancement award from the Judith and Stewart Colton Center for Autoimmunity at NYU Langone Health. Also funding the study were a Cancer Center Support Grant P30CA016087, NIH grant S10OD021727, the NYU melanoma SPORE and NIH R37CA273333, and an NIH/NIAMS T32 grant (AR069515-07). The biophysical analysis part of this work was also supported by multiple grants from National Science Foundations of China (32090044, T2394512, 32200549, and T2394511).

Dr. Wang, Du and You are listed as inventors of pending patents related to the study. NYU Langone Health and its Technology Opportunities & Ventures have formed a related startup company, Remunix Inc., with Dr. Wang as founder and shareholders, to license and commercialize the patents. In addition, Dr. Wang serves as a consultant for Rootpath Genomics, Bristol Myers Squibb, LAV, Regeneron, and Hanmi. Dr. Koide has reported interests in Aethon Therapeutics and Revalia Bio not related to this study. These relationships are managed in keeping with the policies of NYU Langone Health.

Demonstrating that the best solution is not always a multistage approach, a new trial shows catheter ablation is superior to a combination of antiarrhythmic drugs and lifestyle changes — weight loss, more exercise, and alcohol reduction — when treating atrial fibrillation (AF) in patients who also have obesity.

The PRAGUE-25 trial, led by Pavel Osmancik, MD, PhD, with the Cardiocenter at Charles University in Prague, found catheter ablation was roughly twice as effective in an intention-to-treat analysis at controlling AF at the 1-year mark compared with a combination of antiarrhythmic drugs and lifestyle modification (73% vs 34.6%).

A “referral to [catheter ablation] in this population should not be delayed until the patient loses weight,” according to the researchers, who published their findings online on June 30 in the Journal of the American College of Cardiology simultaneously with a presentation at theNew York Valves 2025 Conference.

Obesity: A Strong Predictor of AF

AF, the most common sustained heart arrhythmia, affects about 60 million people worldwide. Obesity is one of its strongest predictors. An increase in BMI of 5 has been linked with a 19%-29% higher incidence of the rhythm disorder.

The PRAGUE trial was a randomized, noninferiority trial conducted in five centers in the Czech Republic. Patients that were included had symptomatic AF (paroxysmal, persistent, or long-standing persistent) and a BMI of 30 to 40.

Patients were randomly assigned 1:1 either to receive catheter ablation (n = 100) or a combination of medication and lifestyle changes (n = 103) from May 2021 to November 2023. Baseline characteristics were balanced, according to the researchers.

After randomization, all patients had a baseline cardiopulmonary exercise test, echocardiography, quality of life analysis, blood biochemistry testing, and a baseline 7-day electrocardiographic Holter recording.

Patients in the catheter ablation group underwent ablation within 6 weeks of randomization. Lifestyle modification was started within 4 weeks after randomization and was managed by teams of dietary specialists and physiotherapists, rather than cardiologists.

Patients in the combination therapy group lost significantly more weight at 12 months (about 6 kg, P < .001 compared to 0.35 kg in the other group), and that weight loss was maintained through the 24-month follow-up. The weight loss goal in this trial was 10%, an ambitious target in the period, especially given the physical limitations associated with AF.

Ramesh Hariharan, MD, cardiac electrophysiologist at UTHealth Houston and Memorial Hermann Health, Houston, who was not part of the study, said much of this research was conducted before the widespread use of GLP-1 receptor agonists, and those medications may help current patients achieve greater weight loss faster.

But even with greater weight loss, Hariharan said, the new findings reinforce the idea that no option alone is enough. Lifestyle changes and medicines need to accompany ablation, not replace it, he said, “otherwise we’re going to end up doing [ablations] more frequently.”

What’s more, technology has improved in the last year with nonthermal pulsed field ablation, which offers “far fewer collateral damage complications” and results in a 45-minute procedure “compared to a 2- to 4-hour procedure before. It has made ablation a lot easier.”

Gregory M. Marcus, MD, MAS, associate chief of cardiology for research at 
UCSF Health, San Francisco, said the evidence “is already definitive that catheter ablation is superior to antiarrhythmic drugs, and there is evidence that successful lifestyle change can reduce the burden of atrial fibrillation.” But this trial is the first to show a head-to-head comparison of ablation with a combination of antiarrhythmic drugs and lifestyle changes.

Marcus said he is not convinced the findings exclude the possibility some in this patient population may still be able to treat their AF without ablation.

“For an obese, very sedentary person who drinks too much alcohol, those are, at least theoretically, the prime candidates for lifestyle modification as a way to effectively treat their Afib,” he said.

One important lesson, Marcus said, is that this adds to the growing evidence that when considering the population at large with AF, “on average, catheter ablation is pretty definitively the most effective way to reduce the chance of atrial fibrillation recurrence.”

But some of the most interesting results were in the group who underwent lifestyle modification, he said. In addition to weight loss and improved exercise capacity, they experienced a statistically significant decrease in hemoglobin A1c concentrations of 1.4 mmol/L compared with an increase of 2.5 mmol/L in patients who received catheter ablation. “Those are things that will prolong life and will also improve quality of life,” he said.

“Whether we’re going to do an ablation or not,” Marcus added, “we should always counsel our atrial fibrillation patients about healthy lifestyle management. There are other things to life besides atrial fibrillation.”

The study authors and Hariharan reported no relevant financial disclosures. Marcus is a consultant and was a co-founder of the startup InCarda Therapeutics, which is investigating a novel therapy for the treatment of acute AF.

Marcia Frellick is an independent, Chicago-based healthcare journalist and a regular contributor to Medscape.

Researchers at Virginia Tech’s Fralin Biomedical Research Institute are developing a method to deliver creatine directly to the brain using focused ultrasound. The technique is being investigated as a potential intervention for children with creatine transporter deficiency, a condition that can impair speech, memory, and learning.

Creatine plays a role in cellular energy production and neurotransmitter regulation, making it critical not only for muscle but also brain function. While oral supplements often improve muscle mass in patients with creatine deficiency, they do not consistently address neurological symptoms, in part because creatine has difficulty crossing the blood-brain barrier.

“Creatine is very crucial for energy-consuming cells in skeletal muscle throughout the body, but also in the brain and in the heart,” says Chin-Yi Chen, a research scientist working on the project.

Ultrasound delivery to bypass the blood-brain barrier

The research is led by assistant professor Cheng-Chia “Fred” Wu, who studies therapeutic focused ultrasound, a noninvasive technique that uses sound waves to temporarily open the blood-brain barrier. The goal is to allow beneficial compounds, like creatine, to reach brain tissue without damaging surrounding cells.

The project, supported by a $30,000 grant from the Association for Creatine Deficiencies, builds on Wu’s broader work using ultrasound to improve drug delivery for pediatric brain cancer. His collaboration with Dr. Seth Berger of Children’s National Hospital led to the idea of applying the same method to treat creatine deficiency.

“Through the partnership between Virginia Tech and Children’s National Hospital, I was able to present our work in focused ultrasound at the Children’s National Research & Innovation Campus,” says Wu. “There, I met Dr. Seth Berger, a medical geneticist, who introduced me to creatine transporter deficiency. Together, we saw the promise that focused ultrasound had to offer.”

Collaboration supports early-stage translational research

Both Virginia Tech and Children’s National have been named Centers of Excellence by the Focused Ultrasound Foundation, a designation that supports collaborative research bridging lab studies and clinical applications. Chen’s initial work will focus on whether creatine can be successfully delivered across the blood-brain barrier and restore normal brain mass in lab models.

“It was a moment that made me really excited — that I had found a lab where I could move from basic research to something that could help patients,” says Chin-Yi Chen. “When Fred asked me, ‘Are you interested in this project?’ I said, ‘Yes, of course.’”

Fitness coach Navneeth Ramprasad, on April 11, shared an Instagram post and explained how avoiding healthy foods can worsen diabetes in your parents. “If your parents are diabetic and you’re not giving them these 5 foods every day, be prepared to spend a lot more on medical bills in a few years, especially the last one. Let’s be real: Most Indian households are still eating the same food that made us the diabetes capital of the world,” Navneeth added.

According to him, here are five foods that your parents must consume every day, if they are diabetic.

1. Fresh coconut and almonds

First thing in the morning, instead of tea or coffee. The healthy fats stabilise blood sugar, reduce morning crashes, and support brain health. Have 2 pieces of coconut and 5 soaked almonds. That’s it. Also read | Diabetes: 7 high-fibre foods that can prevent blood sugar spikes

2. Oats, Greek yoghurt and berries

For breakfast, instead of dosa, idly, or toast. Low GI carbs + protein + fiber + antioxidants = no sugar spikes and longer fullness.

3. Millet khichdi, sprouts and cooked veggies

For lunch, instead of white rice, sambar, and papad. Use foxtail millet or quinoa with moong dal, add steamed sprouts, and a bowl of high fiber veggies. Balanced plate = fiber, protein, slow carbs, and better post-lunch sugar control.

4. Tofu or tempeh for dinner

High-protein, low-carb, and essential for reversing insulin resistance. Add veggies, stir-fry or grill — just don’t end the day with wheat rotis alone.

5. Pumpkin seeds, just before bedtime (9–9:30 PM)

Prevents midnight sugar dips, supports sleep and magnesium levels. 1 small spoon (not more) of raw or lightly roasted seeds is perfect for diabetics who wake up tired or with sugar crashes at night. Also read | Smart eating for diabetes: Nutritionist-approved diet tips to keep your blood sugar in check

Note to readers: This article is for informational purposes only and not a substitute for professional medical advice. Always seek the advice of your doctor with any questions about a medical condition.

A UCSF analysis has found that the newer generation of much more effective diabetes medications are reaching only a fraction of the patients who are recommended to take them based on new guidelines.

Type 2 diabetes (T2D), a condition in which the body can’t use insulin to clear sugar from the bloodstream, affects 1 in 10 Americans. It comes with grave health risks, including cardiovascular and kidney disease.

The study assessed medications that patients received within a year of T2D diagnosis. During the period under review – 2014 to 2022 – groups like the American Diabetes Association and the American Heart Association began encouraging the use of newer medications over some older, less effective ones.

The analysis, which is based on more than 40,000 records from the University of California Health Data Warehouse, found some encouraging results. 

The use of sodium-glucose cotransporter 2 (SGLT2) inhibitors or glucagon-like peptide 1 (GLP-1) receptor agonists – two newer categories of drugs – increased, particularly among patients with cardiovascular or kidney disease.

Meanwhile, the use of sulfonylureas – a category of diabetes drug with severe side effects, now seen as a last resort in treatment – declined. And the use of metformin and insulins, the classic medications for diabetes, declined slightly. 

Still, by 2022, just 20% T2D patients were receiving GLP-1 drugs within a year of diagnosis, and less than 15% of patients were receiving SGLT2 drugs – reflecting a gap between what the professional guidelines recommend and the care that patients are receiving.

The researchers gave several reasons for why this might be. One is that GLP-1 drugs, like Wegovy and Ozempic, are expensive, and insurance doesn’t always cover them. Another is that not every provider knows that leading organizations recommend prescribing GLP-1 and SGLT2 drugs, like Jardiance or Farxiga, for T2D from the moment of diagnosis. 

Some of the most devastating consequences of diabetes come from its effects on the heart and kidney, and thankfully, we now have drugs that target those effects head on. But to maximize the benefit for the many hundreds of thousands of patients in the U.S., we need to increase access to these drugs and make sure that clinicians understand just how beneficial they are.” 

Jonathan Watanabe, PharmD, MS, PhD, the senior author of the study