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Category: biotech/medical – Page 9

The mainz resilience assessment in childhood cancer (MRAcc): development of a novel age-specific patient-reported outcome measure to assess resilience in childhood cancer patients

During intensive cancer treatment, children, adolescents and young adults are exposed to numerous toxicities and psychosocial stressors that can cause psychosocial distress and impair mental health. The maintenance or rapid recovery of mental health during and after exposure to significant stressors has been defined as resilience. To date, resilience research has focused primarily on cross-sectional assessment of specific, trait-like resilience factors and concepts in long-term survivors of childhood cancer, typically omitting the influence of context-specific biopsychosocial stressors and resilience dynamics throughout treatment. Little is known about outcome-based resilience and mental health resources in childhood cancer patients undergoing cancer treatment. In addition, specific instruments for age-appropriate assessment of resilience in childhood cancer patients are lacking. To address this gap, within the EU Horizon 2020-funded FORTEe project, we developed a novel self-report instrument for longitudinal assessment of resilience in children, adolescents, and young adults with cancer, featuring age-appropriate items tailored to their specific contexts.

An interdisciplinary team of psychologists, psychiatrists and pediatric oncologists developed an age-appropriate self-report instrument to assess resilience longitudinally in children, adolescents, and young adults undergoing cancer treatment. Following current resilience research frameworks, resilience is defined as the ratio of changes in mental health problems to stressor exposure. Accordingly, the measure comprises two domains: mental health problems (anxiety, depression, distress, fatigue) and stressor exposure (daily hassles, cancer-related stressors), with stressors rated for both frequency and intensity.

The Mainz Resilience Assessment in Childhood Cancer (MRAcc) consists of three age-specific versions (children 5–11 years, adolescents 12–17 years, young adults 18–21 years), each including the sections: ‘Emotions & Distress’, ‘Fatigue’, and ‘Situations & Experienced Stress’. It is available in German and English and uses either five-point-Likert scales or visual analogue scales presented as thermometers.

Long non-coding RNA may be a promising therapeutic target for cancer

Northwestern Medicine scientists have discovered that a specific long non-coding RNA activates oncogenic signaling pathways in prostate cancer cells and drives tumor progression, underscoring its potential as a therapeutic target, according to a recent study published in Nature Communications. Rendong Yang, Ph.D., associate professor of Urology and a member of the Robert H. Lurie Comprehensive Cancer Center of Northwestern University, was co-corresponding author of the study.

Long non-coding RNAs (lncRNAs) are a type of RNA with transcripts that contain more than 200 nucleotides and play a central role in regulating gene expression, most notably in cancer progression. While previous work has identified many cancer-associated lncRNAs, the mechanisms by which lncRNAs influence cancer progression have remained unknown due to lncRNAs’ cell type-specific and tissue-specific gene expression patterns.

In the current study, the scientists aimed to uncover cellular interactions between super-enhancers—clusters of regulatory DNA elements that drive high levels of transcription—and lncRNAs by studying RNA sequencing data from patients with metastatic castration-resistant prostate cancer.

Alzheimer’s Risk Gene Alters Brain Activity Early — But It May Be Reversible

Carrying one or two copies of the APOE4 gene variant significantly increases the risk of developing Alzheimer’s, and a new study reveals how APOE4 can change neuron activity – potentially many years before symptoms such as memory loss start showing.

In young mice bred to have the APOE4 gene, researchers found specific neurons were smaller and more hyperactive in parts of the brain’s memory center, the hippocampus.

What’s more, they were able to identify a protein, Nell2, contributing to the disruption – and a potential pathway to reverse the damage in advanced cases.

Aging human breast atlas reveals cancer susceptibility

The team used advanced imagining techniques to analyse breast tissue from more than 500 women aged 15 to 86 years old. The tissue included biopsies taken from women for non-cancer-related reasons.

Combining these images with details of the hormone receptors and immune cells present, as well as the tissue architecture, the researchers were able to map how breast tissue changes over time in unprecedented detail. Their findings point to reasons why breast cancer risk increases with age and why tumors in younger women differ biologically.

The author added: “Our map revealed that as women age, their breast tissue goes through major changes, with the most dramatic changes occurring at menopause. There are changes, too, during their twenties, possibly linked to pregnancy and childbirth, but these are far less pronounced.”

The map revealed that all types of cells become fewer in number and divide far less often. Milk-producing structures known as lobules shrink or disappear, while the ducts that that carry milk become relatively more common, with the supporting layer around them becoming thicker. Fat cells increase while blood vessels decrease.

Meanwhile, changes occur in the immune environment. Younger breasts have more B cells and active T cells, which helps them identify and kill cancer cells. As tissue ages, these types of cells decline in number, replaced by other types of immune cell that indicate a more inflammatory and potentially less protective immune environment. ScienceMission sciencenewshighlights.

Scientists have created the most detailed map to date, comprised of over 3 million cells, showing how breast tissue changes as women age – including dramatic changes during menopause.

Continue reading “Aging human breast atlas reveals cancer susceptibility” | >

Tau mutation drives autophagy-lysosome dysfunction

The researchers studied a specific mutation in a brain protein called tau that causes the protein to become misfolded and alter its normal function. In general, when tau proteins become misfolded, they build up inside neurons and contribute to various forms of dementia, including Alzheimer’s dementia and frontotemporal dementia, a neurodegenerative disease similar to Alzheimer’s that often strikes earlier — in middle age — and typically involves significant changes in personality and behavior that precede cognitive decline.

In this new study, the researchers studied neurons that had been reprogrammed from skin cells sampled from patients with frontotemporal dementia who carried the tau mutation. In the neurons, the mutated tau proteins caused waste-recycling centers called lysosomes, which are involved in autophagy, to become dysfunctional, allowing cellular waste to accumulate in the lysosomes, which may contribute to neuronal death. The researchers found that enhancing autophagy with an analog of the chemical compound G2 improved clearance of the garbage, reduced tau levels in the lysosomes and prevented cellular toxicity and death.

G2 was discovered in 2019 via screening experiments seeking drugs that could reduce the accumulation of an aggregation-prone protein in a C. elegans model of alpha-1-antitrypsin deficiency, which can cause severe liver disease. The compound was later shown to boost autophagy function in mammalian cell model systems.

The researchers also have shown that G2 can protect brain cells from death in cells modeling Huntington’s disease, a fatal inherited neurodegenerative disease caused by a genetic mutation present at birth. In the cellular model of Huntington’s disease, the compound prevented the buildup of a harmful RNA molecule. ScienceMission sciencenewshighlights.

New research adds to growing evidence that helping brain cells break down and eliminate their own cellular waste is a promising treatment strategy for a variety of neurodegenerative diseases. In lab experiments, the researchers found that exposure to a novel compound can clear a harmful protein from human neurons modeling frontotemporal dementia — a devastating and ultimately fatal condition — and prevent those neurons from dying.

The study is published in the journal Nature Communications.

Continue reading “Tau mutation drives autophagy-lysosome dysfunction” | >

Body-focused mind-wandering associated with better mental health outcomes, finds new study

Most of us have experienced that when our body is still and resting, the mind doesn’t stop. Instead, it takes off on its own journey of generating thoughts about our past, our plans, and the people around us, a process known as mind-wandering. While researchers have learned a lot about these kinds of thoughts, there aren’t many studies that explore how often our attention turns inward, toward sensations in our bodies, such as our breathing, heartbeat, or physical feelings.

This lesser-known side of our inner experience, called body-wandering, is what a recent study by a brain research team with collaborators from Denmark, Canada and Germany set out to explore.

To understand how the mind focuses on the physical self, researchers conducted a large-scale study with 536 participants who were asked to stay still in the MRI machine during a brain scan while looking at a cross on the screen above them.

How does the most common cause of Alternating Hemiplegia of Childhood (AHC) lead to abnormal repolarization and arrhythmogenesis?

Andrew P. Landstrom & team propose a Ca2+-mediated mechanism in ATP1A3-D801N carriers & identify NCX1 as a possible therapeutic target.

1Department of Cell Biology and.

2Department of Pediatrics, Division of Cardiology, Duke University School of Medicine, Durham, North Carolina, USA.

3Department of Biomedical Engineering and.

4Division of Pediatric Neurology and Developmental Medicine, Department of Pediatrics, Duke University, Durham, North Carolina, USA.

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