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Antimicrobial resistance (AMR) presents a serious challenge in today’s world. The use of antimicrobials (AMU) significantly contributes to the emergence and spread of resistant bacteria. Companion animals gain recognition as potential reservoirs and vectors for transmitting resistant microorganisms to both humans and other animals. The full extent of this transmission remains unclear, which is particularly concerning given the substantial and growing number of households with companion animals. This situation highlights critical knowledge gaps in our understanding of risk factors and transmission pathways for AMR transfer between companion animals and humans. Moreover, there’s a significant lack of information regarding AMU in everyday veterinary practices for companion animals. The exploration and development of alternative therapeutic approaches to antimicrobial treatments of companion animals also represents a research priority. To address these pressing issues, this Reprint aims to compile and disseminate crucial additional knowledge. It serves as a platform for relevant research studies and reviews, shedding light on the complex interplay between AMU, AMR, and the role of companion animals in this global health challenge. This Reprint is especially addressed to companion animal veterinary practitioners as well as all researchers working on the field of AMR in both animals and humans, from a One Health perspective.

Neutrophils, one of the immune system warriors that were thought to be all the same, turn out to be diverse. Unfortunately, these cells are also active in autoimmune diseases. New research has found that a certain subpopulation of these white blood cells can predict disease relapse at an early stage, which may enable improved personalized treatment.

In a study published in Nature Communications, a multi-institutional research team investigated which cell types dominate the blood of patients at the early stage of anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis, which is caused by inflammation in the blood vessels and can disrupt organ function.

“Figuring out the mechanism of this disease, which is poorly understood, will help us understand autoimmune dysregulation in neutrophils. This could aid in the development of new drugs tailored for each patient,” says the lead author of the study. “Because we want to understand the dynamics of neutrophil behavior at the cell level in the early stages of the disease, for this study we recruited new patients that had not yet been treated.”

Macrophage adenosine monophosphate-activated protein kinase (AMPK) limits the development of experimental colitis. AMPK activation inhibits NADPH oxidase (NOX) 2 expression, reactive oxygen species (ROS) generation, and pro-inflammatory cytokine secretion in macrophages during inflammation, while increased NOX2 expression is reported in experimental models of colitis and inflammatory bowel disease (IBD) patients. Although there are reductions in AMPK activity in IBD, it remains unclear whether targeted inhibition of NOX2 in the presence of defective AMPK can reduce the severity of colitis. Here, we investigate whether the inhibition of NOX2 ameliorates colitis in mice independent of AMPK activation. Our study identified that VAS2870 (a pan-Nox inhibitor) alleviated dextran sodium sulfate (DSS)-induced colitis in macrophage-specific AMPKβ1-deficient (AMPKβ1LysM) mice.

Background and ObjectivesIn patients with acute ischemic stroke (AIS), the impact of hemorrhagic transformation (HT) after endovascular treatment (EVT) on poorer stroke outcome is well established when associated with clinical deterioration. However, the…

Just a few weeks after conception, stem cells are already orchestrating the future structure of the human brain. A new Yale-led study shows that, early in development, molecular “traffic cops” known as morphogens regulate the activation of gene programs that initiate stem cells’ differentiation into more specialized brain cells.

The Yale team found that sensitivity to these signaling morphogens can vary not only between stem cells from different donors, but between stem cells derived from the same individual.

“This is a new chapter in understanding how we develop and how development can be influenced by genomic changes between people and by within individuals,” said Flora Vaccarino, the Harris Professor in the Child Study Center at the Yale School of Medicine (YSM) and co-senior author of the research, published in the journal Cell Stem Cell.

An FDA-designated orphan drug that can target a key vulnerability in lung cancer shows promise in improving the efficacy of radiation treatments in preclinical models, according to a study by UT Southwestern Medical Center researchers. The findings, published in Science Advances, suggest a new way to enhance the response to radiotherapy by inhibiting DNA repair in lung cancer cells.

“This study was motivated by challenges faced by millions of cancer patients undergoing radiation therapy, where treatment-related toxicities limit both curative potential and the patient’s quality of life,” said principal investigator Yuanyuan Zhang, M.D., Ph.D., Assistant Professor of Radiation Oncology and a member of the Harold C. Simmons Comprehensive Cancer Center at UT Southwestern.

Prior research, including from the laboratory of co-investigator Ralph J. DeBerardinis, M.D., Ph.D., Professor and Director of the Eugene McDermott Center for Human Growth and Development, Professor in Children’s Medical Center Research Institute at UT Southwestern, and co-leader of the Cellular Networks in Cancer Research Program in the Simmons Cancer Center, has demonstrated that altered metabolic pathways in allow them to survive, grow, and spread. But the role of metabolism in enhancing radiation efficacy has not been thoroughly explored.

Human beings exhibit marked differences in habits, lifestyles and behavioral tendencies. One of these differences, known as chronotype, is the inclination to sleep and wake up early or alternatively to sleep and wake up late.

Changes in society, such as the introduction of portable devices and video streaming services, may have also influenced people’s behavioral patterns, offering them further distractions that could occupy their evenings or late nights. Yet past studies have found that sleeping and waking up late is often linked to a higher risk of being diagnosed with , such as depression and , as well as poorer physical health.

Understanding the neurobiological underpinnings of humans’ chronotypes, as well as the possible implications of being a so-called “morning person” or “night owl,” could thus be beneficial. Specifically, it could inform the development of lifestyle interventions or designed to promote healthy sleeping patterns.

A specialized model used by researchers is becoming a valuable tool for studying human brain development, diseases and potential treatments, according to a team of scientists at Rutgers University-New Brunswick.

Known as chimeric brain models, these laboratory tools provide a unique way to understand human brain functions in a living environment, which may lead to new and better therapies for , researchers said in a review article in Neuron.

Scientists create models by transplanting human brain cells culled from into the brains of animals such as mice, thereby creating a mix of human and animal brain cells in the same brain. This environment is closer to the complexity of a living human brain than what can be simulated in a petri dish study.