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On July 16, 2025, from 9:00 am to 11:00 am (Washington DC time or EDT), join us on the Transatlantic Dialogue on Climate and Health Impacts in Situations of Vulnerability, the fourth in a series of a joint initiative by WHO/Europe and the Pan American Health Organization (PAHO).

This 4th session focuses on climate change and health equity, and will provide input to develop a summary for policy-makers on advancing health equity-oriented approaches for climate action for Member States on both sides of the Atlantic.

This Dialogue aims to:

• Share knowledge on the differential impacts of climate change among population groups across countries and regions, including exposure, vulnerability and coping capacity.
• Exchange experiences on successful interventions that integrate health equity in climate action while acknowledging common and region-specific challenges.
• Foster a collaborative dialogue and stimulate further collaboration towards actionable policy recommendations and strategies that integrate a health equity lens.

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How to participate

• WHEN: Wednesday, 16 July 2025
• TIME: 9:00 a.m. (Washington, D.C., EDT), 3:00 pm (Geneve, Madrid)
• LANGUAGES: Spanish and English

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Context

Climate change has become an undeniable driver of adverse health outcomes worldwide, with evidence mounting on its multifaceted impacts. However, the burden of climate-related health risks is not evenly distributed. Populations more likely to be affected are those exposed to higher risks due to social, economic and environmental factors, including socioeconomic deprivation, geographic location and occupational exposure. 

Populations in situations of vulnerability (as well as children, pregnant women, older adults, ethnic minorities and those living in low-lying coastal or flood-prone areas) face disproportionate impacts, compounded by social determinants that limit their capacity to cope and adapt. This differential vulnerability underscores the critical importance of integrating health equity into climate and health action. Despite increasing awareness of these disparities, most climate–health initiatives have focused broadly on population-wide impacts, often neglecting the specific needs of populations and territories in situations of vulnerability. 

Therefore, there is a necessity to take an equity-based approach, ensuring that adaptation, mitigation and resilience-building efforts explicitly address social inequities, leaving no one behind.

Agenda

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A study published June 25 in the American Journal of Psychiatry provides new insights into a long-standing question in psychiatric research: What is the underlying neurobiological mechanism of psychomotor disturbance in psychiatric disorders?

This study, which explores the relationship between brain connectivity and motor function, reveals a connection between grip strength, well-being and the brain’s default mode network (DMN), offering novel insights for potential clinical applications.

Psychomotor disturbances — ranging from catatonia and psychomotor agitation to disorganized behavior and repetitive movements — are highly prevalent in psychiatric conditions. Despite their high prevalence, the neural mechanisms behind these disturbances have remained elusive.

 

“There has been an exponential increase in the interest to understand psychomotor processes in disease pathology — the fundamental nature of the motor system enhances our ability to link psychological processes to brain to symptoms, promoting clinically useful targets for intervention,” said senior author Alexandra Moussa-Tooks, PhD, an adjunct professor at Vanderbilt University School of Medicine, and co-director of the Clinical and Cognitive Neuroscience Center and head of the Motor Adaptations in Psychotic Disorders Lab at Indiana University Bloomington.

One of the main focuses of this study is the role of grip strength as a measure of both motor function and overall well-being.

“Grip strength is one measure of motor function that has been associated with all-cause mortality and overall well-being,” said first author Heather Burrell Ward, MD, assistant professor of Psychiatry and Behavioral Sciences at Vanderbilt University Medical Center. “It has been assumed that associations between grip strength and well-being are purely related to mechanical impairments reflective of overall poorer physical health.

 

“Therefore, the brain correlates of grip strength have been presumed to lie in the motor system, so previous brain analyses are frequently restricted to motor regions. However, a unifying brain circuit explanation linking grip strength and overall well-being has remained elusive until now. Ours is the first analysis to link grip strength and well-being to alterations in resting-state functional connectivity.”

This study takes a groundbreaking approach by identifying brain regions beyond the motor system that contribute to grip strength and overall health. Using data from the multisite Human Connectome Project for Early Psychosis, which involved 206 participants, including individuals with early psychosis and healthy controls, the researchers applied a data-driven, connectome-wide analysis to uncover the brain circuits associated with grip strength and well-being.

“We observed that higher grip strength was correlated with greater connectivity from multiple brain regions to the DMN,” Ward said.

Given the associations between grip strength and well-being, researchers then repeated this analysis to determine if they would identify similar brain correlates for grip strength and well-being — and they did.

“We identified significant relationships between the same brain regions and their connectivity patterns to the DMN that were related to well-being, overall function and grip strength,” Ward said. “These results have dramatic implications for treatment of psychomotor function in psychotic disorders, as they suggest a unifying role of DMN connectivity in psychomotor disturbance, overall function and well-being.”

Specifically, interventions targeting DMN connectivity could be used to treat psychomotor disturbance and well-being. Repetitive transcranial magnetic stimulation (rTMS) is one form of noninvasive brain stimulation that can be used to modulate DMN connectivity. As director of Neuromodulation Research in the Department of Psychiatry, Ward is currently leading multiple clinical trials that use rTMS to modulate DMN connectivity for people with psychosis.

“These results are exciting because they provide us with novel insights on what brain regions we should target to improve psychomotor function and overall well-being,” Ward said. “With our state-of-the art, fMRI-guided rTMS research at Vanderbilt, we can now test these interventions to develop novel and highly effective treatments for psychosis.”

To learn more, visit www.vumc.org/heatherwardlab.

 

New research from UC Davis Comprehensive Cancer Center has uncovered an evolutionary change that may explain why certain immune cells in humans are less effective at fighting solid tumors compared to non-human primates. This insight could lead to more powerful cancer treatments.

The study was published in Nature Communications. It revealed a tiny genetic difference in an immune protein called Fas Ligand (FasL) between humans and non-human primates. This genetic mutation makes the FasL protein vulnerable to being disabled by plasmin, a tumor-associated enzyme. This vulnerability seems unique to humans and is not found in non-human primates, such as chimpanzees.

The evolutionary mutation in FasL may have contributed to the larger brain size in humans. But in the context of cancer, it was an unfavorable tradeoff because the mutation gives certain tumors a way to disarm parts of our immune system.”

Jogender Tushir-Singh, senior author for the study and associate professor, Department of Medical Microbiology and Immunology

Tumor environment neutralizes key immune protein

FasL is an immune cell membrane protein that triggers a programmed cell death called apoptosis. Activated immune cells, including CAR-T cells made from a patient’s immune system, use apoptosis to kill cancer cells.

The UC Davis team discovered that in human genes, a single evolutionary amino acid change – serine instead of proline at position 153 – makes FasL more susceptible to being cut and inactivated by plasmin.

Plasmin is a protease enzyme that is often elevated in aggressive solid tumors like triple negative breast cancer, colon cancer and ovarian cancer.

This means that even when human immune cells are activated and ready to attack the tumor cells, one of their key death weapons – FasL – can be neutralized by the tumor environment, reducing the effectiveness of immunotherapies.

The findings may help explain why CAR-T and T-cell-based therapies can be effective in blood cancers but often fall short in solid tumors. Blood cancers often do not rely on plasmin to metastasize, whereas tumors like ovarian cancer rely heavily on plasmin to spread the cancer.

Plasmin inhibitors may enhance immunotherapy

Significantly, the study also showed that blocking plasmin or shielding FasL from cleavage can restore its cancer-killing power. That finding may open new doors for improving cancer immunotherapy.

By combining current treatments with plasmin inhibitors or specially designed antibodies that protect FasL, scientists may be able to boost immune responses in patients with solid tumors.

“Humans have a significantly higher rate of cancer than chimpanzees and other primates. There is a lot that we do not know and can still learn from primates and apply to improve human cancer immunotherapies,” said Tushir-Singh. “Regardless, this is a major step toward personalizing and enhancing immunotherapy for the plasmin-positive cancers that have been difficult to treat.”