The research paper explores the multifaceted role of the IL-17 family in immune response, covering everything from infection control to pathological conditions like autoimmune diseases and cancer. Future therapies may exploit IL-17’s unique signaling pathways to offer more targeted and cost-effective treatments.
A team of atmospheric scientists, chemists and infectious disease specialists at the Max Planck Institute for Chemistry, working with colleagues from the Max Planck Institute for Dynamical Systems, the University of Denver, Georg August University and St. Petersburg State University, has embarked on an effort to collate publicly available information on droplet properties, such as the way they are distributed by size, their composition, and the ways they are emitted, as a means of helping to develop mitigation strategies for fighting infectious agents.
In their paper published in the journal Reviews of Modern Physics, the group describes their collating process and why they believe it could help fight non-contact infectious diseases.
In the early days of the pandemic, as people around the world locked themselves inside their residences, scientists, including those not in the medical field, looked for ways to help. One such pair of researchers, Christopher Pöhlker, an atmospheric scientist, and his wife, Mira, a cloud scientist, began to wonder about the nature of droplet size—something related to both their fields of work.
Do you think human beings are the last stage in evolution? If not, what comes next?
I do not think human beings are the last stage in the evolutionary process. Whatever comes next will be neither simply organic nor simply machinic but will be the result of the increasingly symbiotic relationship between human beings and technology.
Bound together as parasite/host, neither people nor technologies can exist apart from the other because they are constitutive prostheses of each other. Such an interrelation is not unique to human beings. As the physiologist J. Scott Turner writes in “The Extended Organism”: “Animal-built structures are properly considered organs of physiology, in principle no different from, and just as much a part of the organism as kidneys, heart, lungs or livers.” This is true for termites, for example, who form a single organism in symbiosis with their nests. The extended body of the organism is created by the extended mind of the colony.
An Australian first biobank will be established to improve and discover new treatments for children with genetic muscle diseases.
The National Muscle Disease Bio-databank, co-led by Murdoch Children’s Research Institute, Monash University and The Alfred, will advance research into our understanding of why children develop genetic muscle diseases.
These diseases, spanning dystrophies and myopathies, are characterised by severe muscle weakness, usually from infancy, that can impact swallowing, breathing and lead to eye problems and learning difficulties.
Housed at Murdoch Children’s, the biobank will store blood test and skin biopsy samples from children across Australia with genetic muscle disease.
Murdoch Children’s Dr Peter Houweling said the project aimed to develop new and better treatments and fast-track discoveries into clinical trials.
So many ways. But one crucial use is to help understand the basis of brain diseases. A reference human brain atlas that describes a normal or neurotypical brain could help researchers understand depression or schizophrenia or many other kinds of diseases, Lein says. Take Alzheimer’s as an example. You could apply these same methods to characterize the brains of people with differing levels of severity of Alzheimer’s, and then compare those brain maps with the reference atlas. “And now you can start to ask questions like, ‘Are certain kinds of cells vulnerable in disease, or are certain kinds of cells causal,” Lein says. (He’s part of a team that’s already working on this.) Rather than investigating plaques and tangles, researchers can ask questions about “very specific kinds of neurons that are the real circuit elements that are likely to be perturbed and have functional consequences,” he says.
What’s the next step?
Better resolution. “The next phase is really moving into very comprehensive coverage of the human and non-human primate brain in adults and development.” In fact, that work has already begun with the BRAIN Initiative Cell Atlas Network, a five-year, $500 million project. The aim is to generate a complete reference atlas of cell types in the human brain across the lifespan, and also to map cell interactions that underlie a wide range of brain disorders.
A kilonova is a bright blast of electromagnetic radiation that happens when two neutron stars or a neutron star and a stellar-mass black hole collide and merge.
When these collisions occur, a vast amount of material is ejected from the neutron stars, the ultradense cores of massive stars that have reached the ends of their lives. This matter is rich in neutral particles called neutrons, and in this violent sea of particles around a neutron star merger, the heaviest elements of the periodic table are forged. These include gold and platinum, radioactive materials such as uranium, and the iodine that flows through our blood. In fact, many pieces of jewelry owe their existence to a kilonova-triggering event.
In a tour de force for neuroscience, teams of researchers have published a voluminous set of brain-cell atlases for humans and other primates.
The atlases are detailed in 21 research papers appearing in Science, Science Advances and Science Translational Medicine — and could point scientists toward new strategies for addressing mental conditions ranging from Alzheimer’s disease and schizophrenia to epilepsy and ADHD.
“We need to understand the specifics of the human brain if we hope to understand human diseases,” Ed Lein, a senior investigator at Seattle’s Allen Institute, said in comments provided via video.
Controlling the adipo-osteogenic lineage commitment of bone marrow mesenchymal stem cell (BMSC) in favor of osteogenesis is considered a promising approach for bone regeneration and repair. Accumulating evidence indicates that oxidative phosphorylation (OXPHOS) is involved in regulating cell fate decisions. As an essential cofactor for OXPHOS, nicotinamide adenine dinucleotide (NAD) has been shown to correlate with the differentiation of stem cells. However, whether NAD manipulates BMSC lineage commitment through OXPHOS remains elusive. Therefore, it is critical to investigate the potential role of NAD on energy metabolism in mediating BMSC lineage commitment.
In this study, the mitochondrial respiration and intracellular NAD+ level were firstly compared between osteogenic and adipogenic cells. For validating the role of NAD in mitochondrial OXPHOS, the inhibitor of NAD+ salvage pathway FK866 and activator P7C3 were used to manipulate the NAD+ level during osteogenesis. Furthermore, a murine femur fracture model was established to evaluate the effect of FK866 on bone fracture repair.
We elucidated that osteogenic committed BMSCs exhibited increased OXPHOS activity and a decreased glycolysis accompanied by an elevated intracellular NAD+ level. In contrast, adipogenic committed BMSCs showed little change in OXPHOS but an upregulated activity in glycolysis and a decline in intracellular NAD+ level in vitro. Moreover, attenuates of NAD+ via salvage pathway in BMSCs diminished osteogenic commitment due to mitochondria dysfunction and reduced activity of OXPHOS. The cells were rescued by supplementing with nicotinamide mononucleotide. In addition, treatment with NAD+ inhibitor FK866 impaired bone fracture healing in vivo.
Patients with advanced/metastatic non–human epidermal growth factor receptor 2 (HER2)-positive gastric/gastroesophageal junction cancer (GC/GEJC) or esophageal adenocarcinoma (EAC) and treated with Opdivo (nivolumab) and chemotherapy maintained their health-related quality of life (HRQoL) “with a reduced risk of definitive deterioration in disease-related and overall health status and without increased treatment-related symptom burden” when compared with patients treated with standalone chemotherapy, according to recent study findings.
Those findings, published in the Journal of Clinical Oncology, “can be helpful when counseling patients with advanced or metastatic GE/GEJC or EAC, providing reassurance that the benefits of adding (Opdivo) to chemotherapy extend not only to improved survival, but also to preservation of their quality of life and prolonged symptom control,” wrote Journal of Clinical Oncology associate editor, Dr. Andrew H. Ko, in a contextual commentary published alongside the study.
Analyzing patient-reported outcomes (PROs) from the phase 3 CheckMate 649 trial, researchers assessed 1,581 participants’ HRQoL via the EQ-5D and Functional Assessment of Cancer Therapy-Gastric (FACT-Ga) scales, including the FACT-General (FACT-G) and Gastric Cancer subscale (GaCS), with the FACT-G GP5 item used to assess treatment-related symptom burden, and studied longitudinal changes in HRQoL measured with mixed models for repeated measures in the PRO analysis population of 1,360 randomly assigned patients, researchers detailed, noting that they also conducted time to symptom or definitive deterioration analyses.