MENOPAUSE IS NOT A DISEASE

Breaking the silence: MyMenoplan.org empowers women to take charge of menopause

Clinical trial shows the NIH-funded website boosts treatment intentions, menopause knowledge and decision-making confidence among users

University of California - San Diego

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Menopause remains one of the most under-discussed stages of life, even though more than 1 million women in the United States experience this natural biological transition each year. Often shrouded in stigma and misinformation, menopause is rarely addressed openly — even though it can profoundly affect a person’s physical, emotional and mental health.

To help bridge this gap, clinicians and researchers who have collaborated on women’s health for over 25 years created MyMenoplan.org. The comprehensive, evidence-based website offers personalized menopause information and decision-making tools designed to empower women to make informed healthcare choices. The website is open and free to everyone and does not require any type of registration or entering of personal information.

“This tool guides a person through a discussion of the symptom, explains why it is common during menopause, and outlines treatment options that may help alleviate it,” said Andrea LaCroix, Ph.D., M.P.H., distinguished professor at the Herbert Wertheim School of Public Health and Human Longevity Science at University of California San Diego and principal investigator of the trial.

In a recent randomized controlled trial published in the journal Maturitas that assessed the impact of MyMenoplan.org, researchers found that women using MyMenoplan.org reported:

• Increased intention to obtain treatment
• Improved menopause knowledge
• Enhanced decision-making progress
• Greater likelihood of revisiting and recommending the website

“One of the unique features of the website is the ‘Create My Menoplan’ tab, where a woman can explore a symptom she’s experiencing, such as hot flashes, night sweats or trouble sleeping,” said LaCroix. “The goal is for women to create their own personalized plan to explore treatments, prepare to speak with their doctors, and try different approaches to feel more comfortable during the menopause transition.”

Implications for Women's Health

Findings from this trial support MyMenoplan.org, the first National Institutes of Health-funded website on menopause, as an effective resource for healthcare providers counseling patients who are experiencing perimenopause (the period of transition into menopause) or postmenopause (defined as having gone more than a year without a menstrual period).

From increased risks of osteoporosis and cardiovascular disease to sleep disturbances and mood changes, the health consequences of untreated or poorly managed menopause can be significant. Yet, due to cultural taboos, lack of education and gaps in medical training, many women navigate this phase without the support or information they need.

“Ideally, when a woman schedules an appointment with their doctor to discuss menopause, her doctor might say, ‘I look forward to speaking with you. Please review this website before your visit and bring any questions you have after reading through the information,’” said LaCroix.

“It's time to break the silence and bring menopause into the public conversation — because awareness is the first step toward better health outcomes.”

Co-authors include: Leslie B. Snyder, University of Connecticut; Katherine M. Newton, Kaiser Permanente Washington Health Research Institute; Hui Xin Ng, UC San Diego; Susan D. Reed, University of Washington School of Medicine; Katherine A. Guthrie, Fred Hutchinson Cancer Center; and Viviana Zambrano, University of Connecticut.

This research was funded, in part, by the National Institutes of Health, National Institute on Aging (5R01AG048209).

Disclosures: The authors do not have any conflicts of interest to report.

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Journal

Maturitas

DOI

10.1016/j.maturitas.2025.108630 

Method of Research

Randomized controlled/clinical trial

Subject of Research

People

Article Title

Positive impact of a menopause website – MyMenoplan.org – on treatment intentions, knowledge, and decision making: A randomized controlled trial

 

Women of African ancestry may be biologically predisposed to early onset or aggressive breast cancers 

University of Notre Dame

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Crislyn D'Souza-Schorey, the Morris Pollard Professor of Biological Sciences at Notre Dame.

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Credit: (Photo by Barbara Johnston/University of Notre Dame)

While the incidence of breast cancer is highest for white women, Black women are more likely to have early-onset or more aggressive subtypes of breast cancer, such as triple-negative breast cancer. Among women under 50, the disparity is even greater: young Black women have double the mortality rate of young white women.

Now research from the University of Notre Dame is shedding light on biological factors that may play a role in this disparity. The study published in iScience found that a population of cells in breast tissues, dubbed PZP cells, send cues that prompt behavioral changes that could promote breast cancer growth.

Funded by the National Cancer Institute at the National Institutes of Health, the study set out to explore what biological differences in breast tissue could be related to early onset or aggressive breast cancers. Most breast cancers are carcinomas, or a type of cancer that develops from epithelial cells. In healthy tissue, epithelial cells form linings in the body and typically have strong adhesive properties and do not move.

The researchers focused on PZP cells as previous studies had shown that these cells are naturally and significantly higher in healthy breast tissues of women of African ancestry than in healthy breast tissues of women of European ancestry. While PZP cell levels are known to be elevated in breast cancer patients in general, their higher numbers in healthy, African ancestry tissues could hold clues to why early-onset or aggressive breast cancers are more likely to occur in Black women.

“The disparity in breast cancer mortality rates, particularly among women of African descent, is multifaceted. While socioeconomic factors and delayed diagnosis may be contributing factors, substantial emerging evidence suggests that biological and genetic differences between racial groups can also play a role,” said Crislyn D'Souza-Schorey, the Morris Pollard Professor of Biological Sciences at Notre Dame and corresponding author of the study.

The study showed how PZP cells produce factors that activate epithelial cells to become invasive, where they detach from their primary site and invade the surrounding tissue.

For example, a particular biological signaling protein known as AKT is often overactive in breast cancers. This study showed that PZP cells can activate the AKT protein in breast epithelial cells, which in part allows them to invade the surrounding environment. PZP cells also secrete and deposit certain proteins outside the cell that guide the movement of breast epithelial cells as they invade.

Overall, the results of the study emphasize multiple mechanisms by which PZP cells may influence the early stages of breast cancer progression and their potential contribution to disease burden.

The researchers also looked at how a targeted breast cancer drug, capivasertib, which inhibits the AKT protein, impacted PZP cells and found it markedly reduced the effects of the PZP cells on breast epithelial cells.

“It’s important to understand the biological and genetic differences within normal tissue as well as tumors among racial groups, as these variations could potentially influence treatment options and survival rates. And consequently, in planning biomarker studies, cancer screenings or clinical trials, inclusivity is important,” said D'Souza-Schorey, also an affiliate of Notre Dame’s Berthiaume Institute for Precision Health and Harper Cancer Research Institute.

D'Souza-Schorey and her lab collaborated with the Indiana University Melvin and Bren Simon Comprehensive Cancer Center’s Susan G. Komen Tissue Bank to access PZP cells and epithelial cells isolated from healthy breast tissues of both African and European ancestry. The cell lines were then grown in a three-dimensional environment, mimicking the way the cells would behave in living tissues and organs.

The research team also worked with the Notre Dame Integrated Imaging Facility for the study.

In addition to D’Souza-Schorey, co-authors include Madison Schmidtmann, Victoria Elliott, James W. Clancy, and Zachary Schafer from Notre Dame and Harikrishna Nakshatri from and IU Simon Comprehensive Cancer Center.

  

Micrograph of PZP cells (green) and breast epithelial cells (red) grown in 3D. 

Credit

(Madison Schmidtmann and James Clancy, D’Souza-Schorey lab.)

Journal

iScience

DOI

10.1016/j.isci.2025.112686 

Subject of Research

Cells

Article Title

Ancestry-linked stromal variations impact breast epithelial cell invasion

LA REVUE GAUCHE - Left Comment: Search results for POINTER SISTERS

Advances in chemistry unlock new pathways for industrial carbon capture, new research finds

Heriot-Watt University

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Professor Mercedes Maroto-Valer, Heriot-Watt UniversityHeriot-Watt University.

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Credit: Heriot-Watt University

Recent key advances in chemistry could tackle emissions from the world’s most polluting industries, according to a new study from a team led by Professor Mercedes Maroto‑Valer, Champion and Director of the Industrial Decarbonisation Research and Innovation Centre (IDRIC) and Director of the Research Centre for Carbon Solutions (RCCS) at Heriot-Watt University, and Dr Steve Griffiths, Professor and Vice Chancellor for Research at American University of Sharjah (AUS).

Published in Nature Reviews Chemistry, one of the world’s most prestigious scientific journals, the paper, titled “Chemistry advances driving industrial carbon capture technologies,” discusses how breakthroughs in chemistry are enabling more efficient and scalable carbon capture solutions for heavy industries such as oil and gas, steel, cement, aluminium and chemicals. Together, these industries account for 40 percent of global greenhouse gas emissions and 85 percent of manufacturing-related emissions.

Carbon capture technology involves capturing CO₂ directly from industrial and energy sources before it enters the atmosphere, then transporting and storing or repurposing it to avoid climate impact. According to the Intergovernmental Panel on Climate Change (IPCC), global carbon capture capacity must increase more than 100-fold—from around 50 million tonnes today to between 4 and 6 billion tonnes annually by 2050—to help limit global warming to 1.5 °C.

While carbon capture technologies are already established in the oil and gas industry, their adoption across other carbon-intensive industries like cement, steel, and chemicals has lagged significantly. This review shows that advances in chemistry are increasingly positioning carbon capture as a viable solution for large-scale industrial decarbonization.

The research highlights innovations including novel amine blends that reduce energy consumption by over 30 percent, metal-organic frameworks (MOFs) that can selectively capture CO2 with extremely high efficiency, and new electroswing technologies that operate at low temperature using renewable electricity instead of energy-intensive heating.

“With heavy industries accounting for a major share of global emissions, advancing these technologies is critical if we’re serious about ever achieving net-zero emissions. Our review highlights the state-of-the-art chemistry behind industrial-scale carbon capture and potential breakthroughs that may further make industrial carbon capture more efficient, scalable and cost-effective. Our aim is for this work to provide the insights necessary for carbon capture to advance at the pace required to achieve global sustainability targets,” said Dr.Griffiths.

The paper reviews five main types of industrial carbon capture technologies—absorption, adsorption, membrane separation, cryogenic gas separation and electroswing systems—and provides insights into how chemistry innovations are improving both their effectiveness and affordability.

“Our work has identified carbon dioxide capture technologies that have progressed to the early stages of development to decarbonise industrial sectors, with a focus on the chemistry that underpins these technologies," said Professor Mercedes Maroto‑Valer.

"We took a global perspective, recognising that carbon capture must be tailored to local contexts. The performance parameters outlined in our research enable industry players to compare materials and technologies more effectively than has previously been possible. We believe this novel approach can help players across both industry and academia pinpoint research opportunities to lower the cost and scale up the commercial deployment of the carbon capture technologies available today."

Additional authors include Prof John M. Andresen from the School of Engineering and Physical Sciences and Dr Jeannie Z. Y. Tan from the Research Centre for Carbon Solutions (RCCS), both at Heriot‑Watt University, as well as Mr Joao M. Uratani from the University of Sussex’s Science Policy Research Unit (SPRU).

This is the second high-profile study in the past year involving researchers from AUS and Heriot-Watt University, following a recent collaboration that proposed green flight paths and the adoption of sustainable aviation fuel as strategies for decarbonising long-haul air traffic.

The published paper is available at www.nature.com/articles/s41570-025-00733-3.

For more information about AUS’ research, visit: www.aus.edu/research.

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Journal

Nature Reviews Chemistry

Article Title

Chemistry advances driving industrial carbon capture technologies

Deep learning-based structural characterization and mass transport analysis of CO2 reduction catalyst layers

Higher Education Press

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Research framework

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Credit: HIGHER EDUCATION PRESS

As global efforts to combat climate change intensify, electrochemical CO₂ reduction reaction (CO2RR) stands out as a critical technology for converting greenhouse gases into valuable fuels and chemicals. Yet, a persistent bottleneck has hindered progress: the lack of precise tools to characterize and optimize the porous catalyst layers where reactions occur. A new study published in Frontiers in Energy resolves this challenge by deploying deep learning (DL) to map microscopic structures and simulate mass transport in CO₂RR catalyst layers with unprecedented accuracy.

 

A research team at Shanghai Jiao Tong University has developed a systematic framework that combines semantic-segmentation AI models with experimental validation to analyze catalyst layers (CLs). Using silver nanoparticles as catalysts and Nafion ionomer as a binder, the team fabricated CLs with varying ionomer-to-catalyst (I/C) ratios (0.2, 0.4, and 0.6) to dissect how composition affects performance.

 

Key Findings

• AI Outperforms Traditional Methods: Among five DL models tested, DeepLabV3plus achieved the highest segmentation accuracy (91.29%), surpassing conventional thresholding techniques (72.35–77.42%). This enabled precise extraction of pore parameters like porosity and pore size distribution, validated against mercury intrusion porosimetry (MIP).
• Optimal I/C Ratio Identified: CLs with an I/C ratio of 0.2 exhibited a twofold increase in gas diffusion distance (672.88 nm vs. 321.38 nm for I/C = 0.6), enabling 89% Faradaic efficiency (FE) for CO production at 250 mA/cm²—the highest reported in the study.
• Structure-Performance Link: Excessive ionomer (I/C ≥ 0.4) clogged macropores, reducing CO₂ accessibility and FE by 12%. Simulations confirmed that lower ionomer content preserved open pore networks critical for long-range mass transport.

 

The integrated framework translates nanoscale morphology directly into device-level performance metrics, providing a scalable blueprint for industrial CO₂ electrolyzers. By minimizing ionomer loading to 0.2, catalyst layers can sustain high current densities without sacrificing selectivity or durability, moving carbon-neutral fuel production closer to market deployment.

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Journal

Frontiers in Energy

DOI

10.1007/s11708-025-1029-x 

Method of Research

Experimental study

Subject of Research

Not applicable

Article Title

Deep learning-based structural characterization and mass transport analysis of CO2 reduction catalyst layers

Article Publication Date

25-Jul-2025

 

Shedding light on why immunotherapy sometimes fails

Researchers discover that some antibody-based therapies can have off-target effects, impairing the immune system’s ability to fight off cancer

Chiba University

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10F.9G2, a monoclonal antibody with high antibody-dependent cellular cytotoxicity, has an off-target effect that involves the reduction of CD8+ T cells. This surpasses the on-target effect, namely programmed cell death protein 1/programmed death-ligand 1 axis inhibition, resulting in no observable antitumor efficacy. In contrast, MIH6, which has low antibody-dependent cellular cytotoxicity activity, exerts only the on-target effect, leading to an effective antitumor response.

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Credit: Assistant Professor Yuta Tamemoto from Chiba University, Japan Source link: https://www.sciencedirect.com/science/article/pii/S0378517325005927?via%3Dihub

Immune checkpoint inhibitors (ICIs), a powerful form of immunotherapy, have revolutionized cancer treatment by unleashing the body’s own immune system to fight tumors. These compounds target the programmed cell death-ligand 1 (PD-L1), a surface protein typically found on tumor cells, which enables the tumors to avoid recognition by immune T cells. By disrupting PD-L1’s function with specially tailored antibodies, ICI-based strategies have brought hope to countless patients with cancer. However, despite their undeniable success, these treatments do not work for everyone. Many patients remain unresponsive to immunotherapy, and scientists have been struggling to understand why some people benefit while others don’t. 

While much research has focused on tumor and patient characteristics that could influence treatment response, less attention has been paid to how the drugs themselves might influence their treatment success. Different antibody drugs, even those targeting the same immune pathway, may have varying properties that subtly or dramatically impact their effectiveness. These include differences in how long they stay in the body, how well they reach tumors, and perhaps most importantly, what other cellular functions they might trigger beyond their intended target.

Against this backdrop, a research team led by Assistant Professor Yuta Tamemoto and Professor Hiroto Hatakeyama from the Graduate School of Pharmaceutical Sciences at Chiba University, Japan, investigated what factors affect the performance of anti-PD-L1 antibodies. Their findings were made available online on May 22, 2025, and were published in Volume 679 of the International Journal of Pharmaceutics on June 30, 2025.

The researchers set out to understand why two different anti-PD-L1 monoclonal antibodies, both designed to block cancer’s immune evasion via the same mechanism, showed vastly different results in laboratory models. In particular, they focused on a powerful immune response called antibody-dependent cellular cytotoxicity (ADCC). Simply put, ADCC is a mechanism that triggers when a cell is covered in antibodies; this elicits a strong immune response that leads to the death of the cell, usually mediated by natural killer cells.

The team compared two specific anti-PD-L1 monoclonal antibodies: MIH6, which has minimal ADCC activity, and 10F.9G2, which exhibits strong ADCC activity. In a mouse tumor model, MIH6 was remarkably effective, inhibiting tumor growth by over 90%. In contrast, 10F.9G2 showed only a slight effect on tumor growth, despite targeting the same immune pathway. Initially, the researchers investigated whether differences in how the antibodies bound to target cells or how they moved through the body could explain this disparity. While MIH6 bound more strongly to cancer cells and remained in the bloodstream longer, these differences alone were not enough to account for the drastic differences in treatment outcomes.

Turning to ADCC as a possible explanation, the researchers discovered that 10F.9G2, the one with strong ADCC activity, unexpectedly reduced the number of antitumor immune cells called CD8+ T cells. This happens because PD-L1, the target of these antibodies, is present not only on cancer cells but also on healthy T cells. When antibodies with high ADCC activity bind to PD-L1 on T cells, they inadvertently trigger the destruction of an essential component of the immune system.

This finding reveals that while ADCC is often a desired secondary mechanism for killing cancer cells in ICI therapies, it can cause a detrimental ‘off-target’ effect when targeting immune checkpoint molecules. “Our results highlight the critical need to consider ADCC activity when designing or selecting antibody therapeutics for immune checkpoint blockade, especially in cancer immunotherapy,” says Dr. Tamemoto.

By shedding light on this unwanted side effect, this study could help scientists improve ICI-based therapies through the careful selection of antibody features based on patient characteristics at the molecular level. “If we assess PD-L1 expression on T cells and determine whether anti-PD-L1 monoclonal antibodies with ADCC activity are appropriate in each case, it may be possible to select the optimal antibodies for each patient,” explains Dr. Tamemoto. “By engineering antibodies that avoid damaging essential immune cells, we may be able to minimize side effects and maximize the effectiveness of cancer immunotherapy.”

Further research efforts into these mechanisms may pave the way for improved cancer treatment.

About Assistant Professor Yuta Tamemoto from Chiba University
Dr. Yuta Tamemoto obtained a PhD degree in pharmacy from the Graduate School of Pharmaceutical Sciences at Chiba University in 2023. He currently serves there as Assistant Professor, conducting research on the topics of life sciences and clinical pharmacy, which includes antibody-based therapies, molecular drug interactions, pharmacokinetics, and pharmacodynamics, among others. He currently has eight scientific publications to his name, with more than 30 citations.

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Journal

International Journal of Pharmaceutics

DOI

10.1016/j.ijpharm.2025.125755 

Method of Research

Experimental study

Subject of Research

Animals

Article Title

Antibody-dependent cellular cytotoxicity of anti-programmed death-ligand 1 antibodies for T cells attenuate their antitumor efficacy in a murine tumor model