Wednesday, July 09, 2025

 

Thick electrodes’ chemistry matters more than structure for battery performance




Rice University
researchers 

image: 

Zeyuan Li and Ming Tang

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Credit: Photo by Jorge Vidal/Rice University





HOUSTON – (July 9, 2025) – Thicker battery electrodes pack in more active materials, promising higher energy density. However, when it comes to lithium-ion battery performance, electrode materials’ thermodynamic properties matter more than their structural design.

A team of Rice University researchers led by materials scientist Ming Tang showed that even if the materials used in thick battery electrodes have nearly identical structures, their internal chemistry impacts energy flow ⎯ and, hence, performance ⎯ differently. This finding goes against conventional wisdom in the field, which holds that creating pore channels in the electrode material via different patterning techniques could mitigate poor reaction uniformity.

“‘Thick’ battery electrodes store more energy, which is great for longer phone life or electric car charge but struggle to charge and discharge quickly due to limited usable capacity,” said Zeyuan Li, a Rice doctoral alumnus and first author on the study. “Imagine trying to fill a thick sponge evenly with water, but the water only rushes into a portion of the sponge, leaving the rest dry ⎯ that is the problem with ‘thick’ electrodes.”

According to a study published in Advanced Materials, the researchers compared two common lithium-ion battery electrode materials ⎯ lithium iron phosphate (LFP) and a nickel manganese cobalt oxide blend known as NMC ⎯ showing the latter performs better despite similar structural characteristics.

“We found that LFP electrodes degraded faster than NMC when tested under identical cycling conditions with more internal cracking and capacity loss due to lopsided lithium flow,” said Li, who now works as a research assistant in the Mesoscale Materials Science Group led by Tang. “If uneven flow was only about pore channels’ dimensions and layout, the electrodes should behave similarly.”

Using high-resolution X-ray imaging at Brookhaven National Laboratory, the researchers tracked where lithium ions traveled inside each electrode during use. The LFP electrodes showed strong reaction “hot spots” near the surface facing the separator — the permeable membrane between a battery’s cathode and anode — while deeper regions remained largely inactive. That unevenness persisted even after resting the battery. In contrast, NMC electrodes had much more balanced reaction profiles.

“We found that the thermodynamic properties of the material dictate how the reaction spreads,” said Tang, associate professor of materials science and nanoengineering at Rice and a corresponding author on the study. “This gives us new insight into battery design and will hopefully play a role in improving efficiencies for thick battery electrodes.”

The findings prompted the team to develop a new metric called the “reaction uniformity number” to help engineers evaluate how well a battery material will perform in thick electrodes. The number captures both structural and thermodynamic factors that influence reaction behavior.

“Batteries that wear out unevenly die faster and waste precious storage capacity,” said Tang, who is also a member of the Rice Advanced Materials Institute. “This discovery provides engineers with new guidance to pick the right recipe in terms of material, microstructure, geometry, etc., for improving thick electrodes’ performance.”

The research was supported by Shell International Exploration and Production Inc., the U.S. Department of Energy (DE-SC0019111, DE-EE0006250, DE-AC02-98CH10886), the National Science Foundation (1626418) and the University of Texas. The content herein is solely the responsibility of the authors and does not necessarily represent the official views of the funding organizations and institutions.


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This news release can be found online at news.rice.edu.

Follow Rice News and Media Relations via Twitter @RiceUNews.

Zeyuan Li

Credit

Photo by Jorge Vidal/Rice University


Peer-reviewed paper:

Probing the Effect of Electrode Thermodynamics on Reaction Heterogeneity in Thick Battery Electrodes | Advanced Materials | DOI: 10.1002/adma.202502299

Authors: Zeyuan Li, Fan Wang, Yuan Gao, Hongxuan Wang, Zhaoshun Wang, Yang Yang, Qing Ai, Mingyuan Ge, Yangtao Liu, Matthew Meyer, Tanguy Terlier, Xianghui Xiao, Wah-Keat Lee, Yan Wang, Jun Lou, Andrew Kiss, Harsh Agarwal, Ryan Stephens and Ming Tang

https://doi.org/10.1002/adma.202502299


About Rice:

Located on a 300-acre forested campus in Houston, Texas, Rice University is consistently ranked among the nation’s top 20 universities by U.S. News & World Report. Rice has highly respected schools of architecture, business, continuing studies, engineering and computing, humanities, music, natural sciences and social sciences and is home to the Baker Institute for Public Policy. Internationally, the university maintains the Rice Global Paris Center, a hub for innovative collaboration, research and inspired teaching located in the heart of Paris. With 4,776 undergraduates and 4,104 graduate students, Rice’s undergraduate student-to-faculty ratio is just under 6-to-1. Its residential college system builds close-knit communities and lifelong friendships, just one reason why Rice is ranked No. 1 for lots of race/class interaction and No. 7 for best-run colleges by the Princeton Review. Rice is also rated as a best value among private universities by the Wall Street Journal and is included on Forbes’ exclusive list of “New Ivies.”

 

Clinical trials reveal promising alternatives to highly toxic tuberculosis drug




Research of Institute of Infectious Diseases and Tropical Medicine at LMU University Hospital Munich and consortium partners shows two novel antibiotics could spare patients from severe side effects




LMU Klinikum





The drugs, sutezolid and delpazolid, have demonstrated strong antimicrobial activity and a notably better safety profile compared to linezolid, with potential to replace this current cornerstone in the treatment of drug-resistant TB. The findings were published on July 8, 2025, in two peer-reviewed articles in The Lancet Infectious Diseases, one of the world’s leading journals in the field of infectious disease medicine. Research partners in Germany included the German Center for Infection Research (DZIF), Munich, the Fraunhofer Institute for Translational Medicine and Pharmacology ITMP, the Center for International Health (CIH) at LMU University Hospital and Helmholtz Munich.

The Challenge with Linezolid

In 2022, the World Health Organisation introduced linezolid as part of the BPaLM regimen, also comprising bedaquiline, pretomanid, and moxifloxacin, as the standard recommended 6-month treatment for patients with multidrug-resistant TB—reducing the duration from the previous standard 18 months. However, linezolid is problematic for patients as it shows significant toxicity. This prolonged exposure to linezolid, much longer than the originally intended use for bacterial skin infections, frequently leads to serious adverse events like anaemia or optical neuropathy, which are distressing for patients, may not resolve fully, and can require discontinuation of therapy, limiting treatment success.

“Despite its effectiveness, linezolid is simply too toxic for many patients. We urgently need safer alternatives in this antibiotic class,” says PD Dr Norbert Heinrich.

Both sutezolid and delpazolid are members of the oxazolidinone class, like linezolid, but are less toxic for patients. In two innovative Phase 2b clinical trials – SUDOCU (PanACEA Sutezolid Dose-finding and Combination Evaluation) and DECODE (PanACEA DElpazolid Dose-finding and COmbination DEvelopment) – both drugs were tested in combination with bedaquiline, delamanid, and moxifloxacin, making them the first trials to use these specific four-drug combinations. The studies, conducted in South Africa and Tanzania, showed that in patients with drug-sensitive pulmonary TB, both drugs are safer and more tolerable for patients than linezolid would be.

Key findings show better patient outcomes

Sutezolid was shown to be effective with strong antibacterial activity and was well tolerated across all tested doses, with no cases of nerve damage or blood toxicity—a critical advantage over linezolid. These results suggest sutezolid could be a safer alternative for future TB treatment regimens, particularly in long-term use, although no final dose recommendation can be made yet.

Delpazolid enhanced the effectiveness of the combination regimen with bedaquiline, delamanid, and moxifloxacin. A once-daily dose of 1200 mg achieved the desired drug levels for maximum efficacy and was well tolerated over 16 weeks. Importantly, no cases of nerve damage or blood-related side effects were observed. These results position delpazolid as a promising alternative to linezolid for future TB treatment regimens—pending confirmation in larger studies.

“These findings suggest that both drugs may offer safer treatment options for TB patients, particularly those requiring longer courses of therapy,” – noted Dr Tina Minja, National PI for the DECODE study at NIMR-Mbeya Medical Research Centre in Tanzania.

A Collaborative Global Effort

The studies were conducted as part of the PanACEA (Pan-African Consortium for the Evaluation of Anti-Tuberculosis Antibiotics) network, which includes clinical and academic partners across Africa and Europe. Both the SUDOCU and DECODE trials were innovative Phase 2b, open-label, randomized clinical studies that systematically compared different dosing levels to evaluate antibacterial activity, drug exposure, and safety profiles of sutezolid and delpazolid.

Looking Ahead

The publication in The Lancet Infectious Diseases underscores the scientific relevance of these results and their potential to shape future TB treatment strategies. “Seeing fewer side effects with sutezolid and delpazolid is a significant step forward—it brings us closer to TB therapies that are both effective and easier for patients to tolerate”, commented Dr Ivan Norena, medical team lead at the Institute of Infectious Diseases and Tropical Medicine at LMU University Hospital Munich.

Further research is now planned to evaluate sutezolid and delpazolid in larger cohorts and in fully optimized treatment combinations. If the promising results are confirmed, these drugs could play a critical role in the next generation of TB therapies, helping to reduce treatment-related side effects while maintaining efficacy.

Funding Acknowledgment

The SUDOCU study was conducted by the PanACEA consortium, funded by the EDCTP2 programme with support from the Federal Ministry of Research, Technology and Space (BMFTR), the German Center for Infection Research (DZIF); Swiss State Secretariat for Education, Research, and Innovation (SERI); Nederlandse Organisatie voor Wetenschappelijk Onderzoek (NWO). Otsuka provided delamanid for this study at no cost to the consortium; and Sequella provided sutezolid active pharmaceutical ingredient at no cost.

Additionally, DECODE was funded by LigaChem Biosciences and the Dutch Research Council (NWO). Otsuka provided delamanid tablets free of charge for this project.

 

Repairing the heart: If zebrafish can do it, why not humans?



Researchers identify genes that help zebrafish regenerate heart muscle, with implications for human therapy



University of California - Berkeley

Neural crest cell reactivation after cardiac injury 

image: 

An uninjured (left) and injured adult zebrafish heart with neural crest cells labeled magenta. Note the neural crest cells activated around the edge of the injury in preparation for regenerating the heart muscle.

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Credit: Megan Martik, UC Berkeley





Humans can't regenerate heart muscle damaged by disease, but scientists have long known that some animals, such as zebrafish, can.

Researchers have now identified a set of genes in zebrafish that reactivate after damage to the heart and patch it up like new, pointing the way to therapies that could reactivate similar genes in humans and jump-start repair of the heart and perhaps other tissues after injury.

The scientists from the University of California, Berkeley, and California Institute of Technology are still working to uncover which upstream gene or genes trigger reactivation of this gene circuit, which normally operates only during development in the embryo. But, once they do, it may be possible to use CRISPR tools to reactivate similar genes in humans after heart damage, since we employ the same set of genes as zebrafish to build the heart during embryonic development.

"Zebrafish and humans are comparable in their cell types and how these cell types form during development, but a major difference in evolution is that adult zebrafish can regenerate many different structures, including their heart, after substantial injury, whereas humans can't," said Megan Martik, a UC Berkeley assistant professor of molecular and cell biology. "How can we harness what nature's already figured out how to do in the zebrafish and apply it in a human context?"

Martik and Marianne Bronner, a Caltech professor of biology and director of the Beckman Institute, are senior authors of a paper about the findings that appeared June 18 in the journal Proceedings of the National Academy of Sciences. The research was led by UC Berkeley graduate students Rekha Dhillon-Richardson and Alexandra Haugan, who are co-first authors of the paper.

The heart is made up of many kinds of cells that comprise muscle, nerve and blood vessel tissue. A portion of these heart cells — in zebrafish, around 12 to 15% — originate from a specific population of stem cells called neural crest cells. Humans have analogous neural crest cells that give rise to varied cell types in almost every organ of the body, ranging from the facial skeleton to the nervous system. Disruption of neural crest cells during development leads to heart defects similar to those found in common congenital heart disorders.

For some reason, zebrafish and a few other animals retain the ability as adults to rebuild tissues derived from the neural crest — the jaw, skull and heart, for example — while humans have lost that ability. These animals are not merely repairing damaged tissue, however. In the heart, cells around an injury revert to an undifferentiated state and then go through development again to make new heart muscle, or cardiomyocytes.

"In both humans and zebrafish, we know that neural crest cells contribute to the heart and that they develop very similarly. But something about them is inherently different on the gene regulatory network level, because the neural crest-derived cardiomyocytes in the zebrafish can respond to injury by regenerating and the same cells in humans can't," Martik said.

CRISPR therapy

In the newly reported research, the scientists used single-cell genomics to profile all the genes expressed by developing neural crest cells in zebrafish that will differentiate into heart muscle cells. They then pieced together the genes expressed after they snipped away about 20% of the fish's heart ventricle. This procedure seemed not to affect the fish, and after about 30 days their hearts were whole again.

By knocking out specific genes with CRISPR, they identified a handful of genes that were essential to reactivation after injury, all of which are utilized during embryonic development to build the heart. One in particular, called egr1, seems to activate the circuit first and perhaps triggers the others, suggesting a potential role in regeneration.

"Differentiated cell types revert back to more of an embryonic gene expression profile and then go through development again," she said. "What we've shown in this paper is that when they do that, they activate this set of genes we know is really important for development of this population of cardiomyocytes."

The researchers also identified the enhancers that turn on these genes. Enhancers are promising targets for CRISPR-based therapies, since they can be manipulated to dial up or down the expression of the gene.

Martik continues to explore the gene circuit involved in regeneration in zebrafish, and has also developed CRISPR techniques to target gene enhancers in heart-like organoids derived from human heart cells. The tiny organoids, called cardioids, are grown in a dish and develop scars similar to normal heart muscle, allowing her team to manipulate the genes involved in repair.

Should she and her colleagues come up with a therapeutic approach, she has a vision that other cells derived from neural crest cells — such as in the jaw or the peripheral nervous system, among others — could be kicked into high gear to stimulate repair.

"There are so many advances, especially here on campus, in terms of CRISPR therapeutics that if we find the switch that can activate the necessary gene programs to drive regeneration in an organism that can regenerate, then I think it'd be completely feasible to develop a CRISPR therapeutic to drive regeneration in a human-derived context," Martik said. "I think Berkeley is the only place something like this can be done."

UC Berkeley assistant specialist Luke Lyons and graduate student Joseph McKenna are also coauthors of the paper. The work was supported by an American Heart Association Career Development Award, the Shurl and Kay Curci Foundation, the National Institutes of Health (K99/R00HD100587, DP2HL173858, T32GM132022, F31HL17614, T32GM148378) and the National Science Foundation (2023360725).

An illustration of zebrafish heart development, showing the migration of cells in the growing embryo after 17 hours, 1 day and 2 days to form the heart. Most heart cells come from the embryonic mesoderm (red) but some 15% come from the cardiac neural crest (green). Neural crest cells also migrate to and become part of the peripheral nervous system and head.

Credit

Hannah Van Mullem, UC Berkeley

Microscope image of the heart of a 2-day-old zebrafish embryo with neural crest cells labeled green. The pumping chambers of the heart, the atrium and ventricle, are labeled.

Credit

Luke Lyons, UC Berkeley