Toggle light / dark theme

That, he says, is when the Universe begins to speak. “We’ve come out of that process and, through ever-deepening complexity, arrived at the ability to understand how it all took place. The Universe, in the form of humans, is now understanding its infancy, its adolescence, and its later stages. We are the place where the whole sequence has become aware of itself.”

“We really need to make use of this empirical knowledge and understand how it can help us in our own lives. How do we grow from it?” asks philosopher of science Nancy Ellen Abrams, speaking with her co-author Joel Primack. “It’s just like with medicine — we don’t make the discoveries, but we get the benefit when we’re sick.” A few thousand people, she notes, have learned to think about the Universe as a whole, based on evidence, not myth. “What people can do with this is reevaluate what we are as human beings.”

That begins, they suggest, with embracing the scale of billions of years — not just as backdrop, but as the substance of our very identity. “We are not a package of organs inside skin,” Abrams says. “We are an embodiment of the history of the Universe, literally history embodied in an incredibly emergent phenomenon here.” Seen this way, our lives gain meaning from deep time.

This review explores the transformative potential of nanotechnology in the treatment and diagnosis of amyotrophic lateral sclerosis (ALS), a progressive neurodegenerative disorder characterized by motor neuron degeneration, muscle weakness, and eventual paralysis. Nanotechnology offers innovative solutions across various domains, including targeted drug delivery, neuroprotection, gene therapy and editing, biomarker detection, advanced imaging techniques, and tissue engineering. By enhancing the precision and efficacy of therapeutic interventions, nanotechnology facilitates key advancements such as crossing the blood-brain barrier, targeting specific cell types, achieving sustained therapeutic release, and enabling combination therapies tailored to the complex pathophysiology of ALS.

Metabolic crosstalk – the exchange of metabolites between cancer cells and non-malignant cells in the tumor microenvironment (TME) – contributes to the aggressiveness of pancreatic ductal adenocarcinoma (PDAC) through a diverse array of mechanisms.

Under the selection pressure imposed by chemical stressors (acidosis, hypoxia) and scarcity of essential nutrients in the TME, PDAC cells establish mutually fitness-enhancing metabolic crosstalk pathways with cancer-associated fibroblasts, tumor-associated macrophages, and other stromal cells.

PDAC cell metabolism inhibits the activity of cytotoxic T lymphocytes and natural killer cells by outcompeting them for essential nutrients (glucose, amino acids, nucleosides, vitamins) and by flooding the TME with immunosuppressive metabolites (lactate, kynurenine, adenosine, and others).

Critical nodes of tumorigenic metabolic crosstalk pathways (enzymes and cell membrane transporters) are readily druggable and likely non-essential for healthy tissues. https://sciencemission.com/Tumor%E2%80%93stromal-metabolic-crosstalk-in-PC


Pancreatic ductal adenocarcinoma (PDAC) is an aggressive malignancy with a dire prognosis. Standard-of-care chemotherapy regimens offer marginal survival benefit and carry risk of severe toxicity, while immunotherapy approaches have uniformly failed in clinical trials. Extensive desmoplasia in the PDAC tumor microenvironment (TME) disrupts blood flow to and from the tumor, thereby creating a nutrient-depleted, hypoxic, and acidic milieu that suppresses the function of antitumor immune cells and imparts chemotherapy resistance. Additionally, recent seminal studies have demonstrated crucial roles for metabolic crosstalk – the exchange of metabolites between PDAC cells and stromal cell populations in the TME – in establishing and maintaining core malignant behaviors of PDAC: tumor growth, metastasis, immune evasion, and therapy resistance.