Tuesday, July 07, 2026

 

Biochar “switches on” natural oxygen chemistry to suppress soil-borne pathogens and reshape healthier microbial communities




Biochar Editorial Office, Shenyang Agricultural University

Biochar modulates soil microbial communities via reactive oxygen species derived from its constituents 

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Biochar modulates soil microbial communities via reactive oxygen species derived from its constituents

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Credit: Meng Liu, Siqi Shen, Haiyang Qiao, Huiqiang Yang, Yaru Zhu, Yawei Zhou & Hanzhong Jia





A new study published in Biochar reveals how specially prepared biochar can directly suppress a destructive soil-borne pathogen while helping rebuild a richer and more stable soil bacterial community. The findings offer a clearer scientific basis for designing biochar amendments that protect crops without broadly damaging beneficial soil life.

Soil-borne diseases remain one of agriculture’s most stubborn challenges. Pathogens such as Ralstonia solanacearum, the bacterium responsible for bacterial wilt in crops including tomato and tobacco, can persist in soil and attack plant roots. Traditional soil disinfection methods can reduce pathogens, but they often act broadly, harming both harmful and beneficial microorganisms. This makes it difficult to maintain long-term soil health.

In the new study, researchers led by Hanzhong Jia investigated whether biochar could provide a more targeted way to manage soil pathogens. The team prepared biochars from four types of straw materials at different pyrolysis temperatures, ranging from 300 to 700 °C, and tested their antibacterial effects against R. solanacearum.

The strongest results came from tobacco stem biochar, which showed powerful antibacterial activity. Biochar made at 300 to 400 °C inhibited the pathogen by 92.91% to 99.60%, while biochar produced at 500 to 700 °C achieved 100% inhibition in laboratory tests.

“Our results show that biochar is not only a passive soil amendment,” said Hanzhong Jia, corresponding author of the study. “By controlling the raw material and pyrolysis temperature, we can tune the reactive chemistry of biochar and use it to suppress pathogens while supporting a healthier microbial community.”

The key lies in reactive oxygen species, or ROS. These oxygen-containing molecules can damage bacterial cells through oxidative stress. The study found that biochar’s ROS profile changed with pyrolysis temperature. At lower temperatures, tobacco stem biochar mainly produced free radical ROS, including hydroxyl radicals and superoxide radicals. At higher temperatures, it mainly contained non-radical ROS, including singlet oxygen and hydrogen peroxide.

This temperature-dependent switch mattered. Quenching experiments, which used chemical scavengers to neutralize different ROS, confirmed that ROS were the principal antibacterial mechanism. When the researchers reduced ROS activity, the biochar’s ability to suppress the pathogen also dropped sharply.

The team then tested whether this effect could protect plants. In hydroponic tomato seedling experiments, plants infected with R. solanacearum showed severe wilting. By contrast, seedlings treated with tobacco stem biochar showed no disease symptoms and maintained growth comparable to healthy controls. When ROS were quenched, the protective effect was largely lost, further confirming the central role of ROS.

Beyond pathogen control, the study found that tobacco stem biochar helped reshape the rhizosphere microbiome. In artificial soil and diseased soil systems, biochar increased bacterial richness and promoted a more complex and stable microbial network. The Chao1 richness index increased by 497.77 to 951.34, while microbial network nodes increased by 82 to 136 and edges increased by 1,224 to 2,185. Beneficial genera such as Rhizobium, Paracoccus, Cellvibrio, Fluviicola, and Pseudomonas became more abundant, while several pathogen-associated or less desirable groups declined.

“These findings help explain why biochar can sometimes improve disease resistance in soil,” Jia said. “The benefit comes not only from changing soil properties, but also from direct ROS-mediated interactions with microorganisms.”

The study provides a practical message for agriculture: biochar performance depends strongly on how it is made. By selecting suitable biomass and pyrolysis temperatures, researchers and growers may be able to design biochar products that reduce soil-borne disease pressure while encouraging beneficial microbial recovery.

The research points toward more precise, microbiome-friendly strategies for sustainable crop protection.

 

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Journal Reference: Liu, M., Shen, S., Qiao, H. et al. Biochar modulates soil microbial communities via reactive oxygen species derived from its constituents. Biochar 8, 122 (2026).   

https://doi.org/10.1007/s42773-026-00637-5   

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About Biochar

Biochar (e-ISSN: 2524-7867) is the first journal dedicated exclusively to biochar research, spanning agronomy, environmental science, and materials science. It publishes original studies on biochar production, processing, and applications—such as bioenergy, environmental remediation, soil enhancement, climate mitigation, water treatment, and sustainability analysis. The journal serves as an innovative and professional platform for global researchers to share advances in this rapidly expanding field. 

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New Columbia Nursing research reveals nurse practitioner workforce growth outpaces projections as physician and physician associate growth remains steady




Columbia University Irving Medical Center






New York, NY (July 7, 2026) ---New Columbia University School of Nursing research reveals nurse practitioner (NP) workforce growth outpaced prior projections while physician and physician associate (PA) growth remained steady between 2016 and 2023. During this period, the NP workforce expanded at an average annual rate of 10%, while physician and PA workforces grew at 1.1% and 8.6% per year, respectively. 

“Given pandemic disruptions to clinician training, early evidence that NP supply may be outpacing prior forecasts, and unprecedented growth in NP jobs, an update to current workforce projections is warranted,” the authors note. 

By 2030, researchers project annual growth of 1.1% for physicians, 11% for NPs, and 5.6% for PAs. These projections position NPs and PAs to help fill critical health care gaps as the U.S. population ages and demand for care grows. Staffing, training, and care policies will need to account for the surge in these health professions, according to the authors.  

The study, “Workforce Projections for Physicians, Nurse Practitioners, and Physician Associates,” was published in Health Affairs on July 7, 2026. 

Cohort-based modelling leads to better insights 

According to the paper, its forecast diverges from the Health Resources and Services Administration projections due to differences in modelling approaches. 

The research team, led by assistant professor Monica O’Reilly-Jacob, PhD, used the Cohort Supply Model to analyze 40 years of census data to separately identify two factors: how likely someone is to work at different life stages, such as during child-rearing years or near retirement, and how likely people born in a given year are to enter a particular profession. This approach treats each year's data independently, so early assumptions do not compound into later projections. 

“Cohort-based modelling is especially useful in capturing workforce dynamics in predominantly female professions, where life-cycle work patterns shape participation and long-term supply,” the authors explain.  

The acceleration of NP workforce growth may be attributed to the challenging work environments registered nurses (RNs) face. Many RNs are turning to graduate degrees to jumpstart careers that offer predictable schedules and greater autonomy. In response, graduate nursing programs are increasing their course offerings and modalities, such as distance learning, which may explain the differences in NP and PA workforce growth.  

Researchers argue that growth in the NP and PA workforces helps position these professions to fill critical care gaps, including providing primary care in underserved communities and for at-risk populations and addressing shortages in certain subspecialties such as psychiatry. 

“Regulations and payment policies should more effectively leverage this growing workforce to address geographic and specialty shortages. Federal, state, and organizational policies should enable NPs and PAs to provide high-quality and cost-effective care. Ongoing monitoring of NP and PA supply and demand, and whether expanding capacity is reaching high-need communities, will be essential as the NP workforce continues its rapid growth,” the authors conclude.  

Other study authors include David Auerbach, PhD, Brandeis University, Heller School of Social Policy & Management; Lusine Poghosyan, PhD, Columbia University School of Nursing; Susan Kelly-Weeder, PhD, George Washington University, School of Nursing; and Sean Clarke, PhD, Emory University, Nell Hodgson Woodruff School of Nursing. 

About Columbia University School of Nursing  

Columbia University School of Nursing is advancing nursing education, research, and practice to advance health for all. As one of the top nursing schools in the country, we offer direct-entry master’s degrees, advanced nursing, and doctoral programs with the goal of shaping and setting standards for nursing everywhere. And, as a top recipient of NIH research funding, we address health disparities for under-resourced populations and advance equitable health policy and delivery.  

Through our expansive network of clinical collaborations in New York City and around the world—including our dedicated faculty practice, the ColumbiaDoctors Nurse Practitioner Group—we cultivate a culture of innovation and diversity and champion a community-centered approach to care. Across the Columbia Nursing community, we encourage active listening, big thinking, and bold action, so that, together, we’re moving health forward.  

Columbia University School of Nursing is part of Columbia University Irving Medical Center, which also includes the Columbia University Vagelos College of Physicians and Surgeons, the Mailman School of Public Health, and the College of Dental Medicine. 

 

Why does Parkinson’s disease affect more men than women?



Study reveals differences in gene activity in the brain



Federation of European Neuroscience Societies

Sex-dependent changes in cell-cell communication events in brains of Parkinson's disease patients 

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Cell-cell communication plot showing how different brain cells communicate with each other in people with Parkinson’s disease compared to individuals without the disease. It highlights that these cell-to-cell interactions change in Parkinson’s, suggesting altered communication in the brain. When looking separately at males and females, the patterns differ, indicating that the disease may affect brain cell communication in sex-specific ways.

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Credit: Please credit Dr Julia Schulze-Hentrich





Barcelona, Spain: New research presented today (Wednesday) at the Federation of European Neuroscience Societies (FENS) Forum 2026 [1] has discovered some of the genetic changes in brain cells that may help to explain why more men than women develop Parkinson’s disease.

 

Parkinson’s disease (PD) is a condition in which parts of the brain become progressively damaged over many years. It affects approximately 9.4 million people worldwide and it is becoming increasingly prevalent, especially as populations age. Around 90% of cases are thought to be caused by a combination of genetic variations and environmental and lifestyle factors. PD is 1.5- to 2-fold more common in men than women, but the reasons for this difference are not clear. Men also experience a faster decline in their thinking abilities and faster progression of difficulties with everyday living.

 

Dr Julia Schulze-Hentrich, a professor in the Genetics and Epigenetics Department and affiliated with the Center for Gender-Specific Biology and Medicine (CGMB) at Saarland University, Germany, told the FENS Forum: “The higher prevalence of Parkinson’s disease in men suggests that sex-dependent biology may influence vulnerability. Therefore, studying sex differences may help identifying disease mechanisms that would be hidden in analyses that pool men and women together.”

 

In earlier work [2], Professor Schulze-Hentrich and colleagues had studied blood samples from agricultural workers, including 71 people with early PD and 147 healthy controls. They found that women with PD had changes to DNA methylation in 69 regions of the genome, compared to only two in men. DNA methylation doesn’t change genes, but works like a dimmer switch to turn the activity of genes up or down.

 

“These findings suggested that a person’s genetic make-up influences these DNA methylation changes, and that interaction with environmental exposures, such as to pesticides, may also contribute to the development of Parkinson’s disease,” she said.

 

In her new research presented today, Prof. Schulze-Hentrich set out to understand the mechanisms that might be playing a role in the different DNA methylation patterns she had seen in men and women and their associations with PD. The researchers looked at post-mortem brain samples from 73 people with PD (28 women and 45 men) and compared them with samples from a control group of 24 people without PD (9 women and 15 men).

 

“We looked at differences in gene expression individually in all cells of the brain – neurons, astrocytes, oligodendrocytes and microglia – in healthy brains and in PD brains in men and women. We studied five brain regions and found that PD causes common changes in the brain, regardless of sex. All these cells in the five regions, showed signs of being under stress. They switched on proteins that help damaged proteins fold correctly, called ‘chaperones’. However, we also found important differences between men and women in gene activity in some cells and some brain regions,” she said.

 

Neurons are the brain’s communication nerve cells, while astrocytes, oligodendrocytes and microglia are glial nerve cells, which provide support and maintenance for the neurons.

 

The researchers found that in astrocytes, the activity of genes linked to mitochondria (the cell’s energy producers) was different between sexes. In oligodendrocytes, the activity of genes involved in making and maintaining the protective coating around nerve fibres (myelin) also differed between sexes. These differences occurred regardless of what region of the brain they were in.

 

“This shows that PD triggers some shared ‘stress responses’ in everyone’s brain cells, but also there are differences between men and women at the cellular level, especially in how the brain ‘support’ cells manage energy and protect nerve connections. Our findings help to explain why symptoms and disease progression in Parkinson’s differ between men and women. Eventually, they may lead to more personalised treatments rather than treating all patients with PD as biologically identical,” said Prof. Schulze-Hentrich.

 

“Most importantly, our results indicate that it is crucial to recognise that biology varies between the sexes in PD research and that, wherever possible, researchers should analyse data separately in males and females instead of pooling everyone together. This is crucial to see whether an association, effect or outcome differs by sex. It also helps identify gaps in evidence because many studies still under-report or pool sex-specific outcomes.

 

“For patients, the main benefit is more personalised care, as sex-specific analysis can help clinicians predict which symptoms are more likely, monitor problems earlier, and choose treatments that fit a patient’s risk profile better.”

 

The discovery of how different cells in the brain function differently between sexes, both healthy and diseased, is a strength of the study and fills a gap left by studies that have focussed just on neurons and males. A limitation is the small number of samples investigated. Prof. Schulze-Hentrich said that a coordinated effort was needed to improve this and investigate greater numbers of samples, stratified by sex.

 

“Investigating how male- and female-specific glial responses shape vulnerability, progression and treatment response is rarely done in a systematic and coordinated way. Therefore, the German Research Foundation (DFG) Priority Programme ‘SEX and GLIA’ starting in the autumn of 2026 will bring together physiologists with functional geneticists and computational biologists to uncover a largely hidden layer of sex-biased biology that previous studies often ignored,” she concluded.

 

Professor Christina Dalla from the National and Kapodistrian University of Athens, Greece, is chair of the FENS Forum communication committee and was not involved in the research. she said: “Although we have known for some time that there are higher rates of Parkinson’s disease in men than in women, it is interesting to see how Professor Schulze-Hentrich and her colleagues have built on their earlier work studying the impact of pesticides on agricultural workers to investigate the changes that occur at the cellular level and to understand the mechanisms underlying the development of Parkinson’s disease.

 

“Their findings show that although some changes in genetic activity are the same in both sexes, there are others that only occur in men, or in women. This is an important finding because it shows that there are differences in glial cells, the ‘support’ cells in the brain that are associated with the onset of the disease, and that these could interact with other factors such as sex, hormones or social or environmental exposures.”

 

(ends)

 

Notes

[1] “Sex differences in glial cells contribute to the molecular etiology of Parkinson’s disease”, by Julia M. Schulze-Hentrich, Cell-Cell Communication and Plasticity scientific symposia, 09:45 – 11:15 hrs CEST, Wednesday 8 July, Hall C:

https://fens2026.abstractserver.com/program/#/details/presentations/164

[2] Schaffner, S.L., Casazza, W., Artaud, F. et al. “Genetic variation and pesticide exposure influence blood DNA methylation signatures in females with early-stage Parkinson’s disease”. npj Parkinsons Dis. 10, 98 (2024). https://doi.org/10.1038/s41531-024-00704-3