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A World Where Anyone Who Needs a Bone Marrow Transplant Gets One — Kevin Caldwell — Ossium Health

Imagine a world where anyone who needs a bone marrow transplant can get one — on demand. No more desperate donor searches or deadly delays. Kevin Caldwell, Co-Founder & CEO, Ossium Health.


Bone marrow transplants have always depended on finding the right donor at the right time. But what if bone marrow could be stored, shipped, and used on demand—just like a drug? That’s exactly what Ossium Health is now showing in human clinical data.

Kevin Caldwell is the Co-Founder, CEO, and President of Ossium Health (https://ossiumhealth.com/), a clinical-stage bioengineering company pioneering off-the-shelf, cryopreserved bone marrow therapies derived from deceased organ donors.

Under Kevin’s leadership, Ossium has developed a novel platform designed to solve one of the most persistent challenges in transplantation medicine: timely access to compatible bone marrow for patients with life-threatening hematologic malignancies such as Acute Myeloid Leukemia. The company’s approach enables on-demand delivery of viable marrow cells, bypassing the logistical and biological constraints of traditional donor matching and scheduling.

Since its founding, Kevin has scaled Ossium from an early-stage startup into a clinical-stage company with a robust network of over 50 strategic partnerships across supply, clinical development, and commercial channels. He has led multiple financings and secured a landmark contract with the Biomedical Advanced Research and Development Authority, validating Ossium’s relevance to national health preparedness and biomanufacturing resilience.

Epigenetic regulation of serine biosynthesis by PHF8 during neurogenesis

Linking epigenetics and metabolism in neurogenesis!

Epigenetic regulation and metabolism are tightly coordinated during progenitor cell growth but the processes linking this crosstalk is not well understood.

The researchers examined in neural stem cells the role of PHF8, a histone demethylase whose mutations are linked to Siderius-Hamel syndrome, a rare neurodevelopmental disorder.

The authors show that PHF8 regulates neural progenitor proliferation by coordinating epigenetic and metabolic programs and drives serine biosynthesis by maintaining chromatin accessibility of serine synthesis genes.

They also demonstrate that loss of PHF8 disrupts metabolism, autophagy, and vesicle formation and its deficiency leads to DNA damage and halts neurogenesis in vivo. sciencenewshighlights ScienceMission https://sciencemission.com/Epigenetic-regulation-of-serine-biosynthesis


Progenitor proliferation during neurodevelopment requires tight coordination of epigenetic regulation and metabolism. However, the crosstalk between these processes remains poorly understood. To investigate this, we examine in neural stem cells the role of PHF8, a histone demethylase whose mutations are linked to Siderius-Hamel syndrome, a rare neurodevelopmental disorder. Through an integrated multi-omics approach — combining transcriptomics, epigenomics, and metabolomics — we identify PHF8 as a key driver of the serine biosynthesis pathway, safeguarding the intracellular serine pool essential for neural progenitor proliferation. PHF8 fine-tunes chromatin accessibility at promoters of metabolic genes, ensuring their activation during development. Loss of PHF8 disrupts amino acid metabolism, blocks autophagy, and hinders vesicle formation.

Nasal swab test spots early Alzheimer’s signals

Schwann cell-derived exosomes are powerful promoters of nerve repair, capable of enhancing axon regrowth, remyelination, and functional recovery in numerous models. These effects are mediated via multifactorial cargo (miRNAs, mRNAs, proteins) that modulate neurons, glia, endothelial, and immune cells. Importantly, what began as a novel biological insight is now rapidly moving toward therapeutic innovation. Schwann cell-derived exosomes thus represent both a novel mode of glia–neuron communication and a promising avenue for next-generation therapies for nerve regeneration.

Natural competition between brain circuits may boost information processing

Over the past decades, neuroscience studies have painted an increasingly detailed picture of the human brain, its organization and how it supports various functions. To plan and execute desired behaviors in changing circumstances, networks of neurons in the brain can either work together or suppress each other, thus employing both cooperative and competitive interaction strategies.

Researchers at University of Oxford, University of Cambridge, McGill University, University of Aarhus and Pompeu Fabra University recently set out to better understand the mammalian brain’s underlying dynamics, specifically how its underlying architecture balances cooperative and competitive interactions between neural circuits. Their paper, published in Nature Neuroscience, offers new insight that could both improve the understanding of the brain and inform the development of brain-inspired computational models.

“Building models of the brain is an important part of modern neuroscience,” Andrea Luppi, first author of the paper, told Medical Xpress. “As Nobel winner Reichard Feynman said, ‘what I cannot create, I do not understand.’ Most current models, however, share a limitation. Everyday experience, from focusing attention or switching between tasks, also reveals that brain systems must compete for limited resources.

Circadian rhythm drives metabolic dysfunction in fat cells, study finds

Northwestern Medicine scientists led by Joseph Bass, MD, Ph.D., the Charles F. Kettering Professor of Endocrinology and Metabolism and director of the Center for Diabetes and Metabolism, have discovered how disruptions in the circadian rhythm impair metabolic function in fat cells, providing new insights into the molecular mechanisms that cause obesity and metabolic disease, according to a recent study published in Nature Metabolism.

“It’s not simply the accrual of excess fat that leads to disease. It’s a change in the actual function and the capacity of the energy center within the cell to work properly,” said Bass, who is also chief of Endocrinology, Metabolism and Molecular Medicine in the Department of Medicine and a member of the Robert H. Lurie Comprehensive Cancer Center of Northwestern University.

The circadian rhythm is the body’s own internal 24-hour clock that regulates the sleep-wake cycle, hormone levels and metabolism, among other systems throughout the body.

Seven subsets, two fates: mouse γδ T cells in cancer immunity

Mouse γδ T cells in cancer immunity.

Mouse γδ T cells are not all the same; rather, they comprise seven subsets that influence progression in several cancer types.

Antitumor γδ T cell subsets can be tissue-resident or circulating cells, which generally rely on glycolysis for energy production, and they mediate cancer cell death via interferon-gamma or orchestration of antitumor immunity.

Protumor γδ T cell subsets use lipids for energy production, and they promote primary tumor growth and metastasis through the production of interleukin17A to modulate the behavior of myeloid cells sciencenewshighlights ScienceMission https://sciencemission.com/Seven-subsets,-two-fates


The importance of γδ T cells in cancer, as defenders against tumorigenesis, was established more than 2 decades ago. Since that time, research using mouse models of cancer has brought to light a nonuniform view of tumor-associated γδ T cells by providing granularity into the role of individual γδ T cell subsets in specific cancer types. In this review, we discuss data that highlight the unique contributions of Vγ1+, Vγ4+, Vγ5+, Vγ6+, and Vγ7+ cells throughout cancer progression. We delve into their responses to tumors, including both protective and pathogenic functions. We examine how the mechanisms by which these mouse immune cell subsets shape tumor development and spread can be exploited for therapeutic purposes in people with cancer.

AI Designed Peptides Could Cure… EVERYTHING. LigandForge Is Here

LigandForge generates 150,000 peptide drug candidates in 3 minutes — a million times faster than existing methods, unlocking a tsunami of possible treatments.

A man with no medical background used ChatGPT, AlphaFold, and Grok to design a custom mRNA cancer vaccine for his dying dog — and her biggest tumor shrank 75%.

Meanwhile, scientists discovered a single protein that literally spreads aging through your bloodstream. These stories are each incredible on their own. But the big story is the implications for curing aging.

In this deep dive, I break down how these three breakthroughs fit together, what peptides and mRNA vaccines actually are (and how they’re different), and why this moment might be the most important inflection point in the history of drug design.

The age of custom AI cures isn’t coming. It’s here.

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