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The Minds That Left Reality | Diaspora

Greg Egan’s Diaspora is one of the most ambitious and mind-bending science fiction novels ever published. It came out in 1997 and originally started as a short story called “Wang’s Carpets.” That story ended up as a chapter in the novel. Diaspora is: dense, smart, and way ahead of its time.
This is hard science fiction to the core. Egan invents entire new branches of physics. He reimagines life, consciousness, time, space — even what it means to be human. The book doesn’t ease you in. There’s a glossary, invented physics theories like Kozuch Theory, and characters that don’t even have genders. But if you stick with it, what you get isn’t just a story, it’s a look at what the future might actually become.
By the year 2,975, humanity isn’t one species anymore. It’s split into three groups: Fleshers: The biological humans, including the “statics” (unchanged baseline humans) and all sorts of heavily modified versions — underwater people, gene-hacked thinkers, even “dream apes” who gave up speech to live closer to nature. Gleisners: AIs in robotic bodies that live in space. They care about the physical world and experience time like regular humans. They’re kind of old-school — still sending ships to the stars, trying to build things in real space. Citizens: These are digital minds that live entirely in simulated worlds called polises.

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Insulin on edge: Study identifies stress-triggered gene behind diabetes

Researchers from Osaka Metropolitan University have identified a gene that, when activated by metabolic stress, damages pancreatic β-cells—the cells responsible for insulin production and blood sugar control—pushing them toward dysfunction. The findings highlight a promising new target for early intervention in type 2 diabetes. The study is published in the Journal of Biological Chemistry.

While many factors can contribute to type 2 diabetes, lifestyle, especially diet, plays a major role in its onset. Genetics matter, but poor eating habits can greatly increase the risk of developing what is now often called a “silent epidemic.”

“Type 2 diabetes occurs when pancreatic β-cells, which secrete insulin to regulate , become impaired due to prolonged stress caused by poor dietary habits, a condition known as ,” said Naoki Harada, an associate professor at Osaka Metropolitan University’s Graduate School of Agriculture and lead author of this study.

Scientists use gene editing to correct harmful mitochondrial mutations in human cells

In a step toward treating mitochondrial diseases, researchers in the Netherlands have successfully edited harmful mutations in mitochondrial DNA using a genetic tool known as a base editor. The results, published in the open-access journal PLOS Biology, offer new hope for people with rare genetic conditions.

Mitochondria have their own small set of DNA. Mutations in this mitochondrial DNA can lead to a wide range of maternally inherited diseases, cancer, and aging-related conditions. While the development of CRISPR technology has given scientists new ways to correct mutations in nuclear DNA, this system cannot effectively cross the mitochondrial membrane and reach mitochondrial DNA.

In the new study, the researchers used a tool called a base editor—specifically, a DdCBE (double-stranded DNA deaminase toxin A-derived cytosine ). This tool allows scientists to change a single letter in the DNA code without cutting it, and it works on mitochondrial DNA.

Fusion superkine and focused ultrasound could enable targeted, noninvasive therapy for glioblastoma

Researchers at VCU Massey Comprehensive Cancer Center and the VCU Institute of Molecular Medicine (VIMM) have discovered a new and potentially revolutionary way to treat glioblastoma (GBM), the most aggressive type of brain cancer, which currently has no curative treatment options.

In a study led by Paul B. Fisher, MPh, Ph.D., FNAI, and Swadesh K. Das, Ph.D., recently published in the Journal for ImmunoTherapy of Cancer, researchers created a that demonstrates the ability to introduce a combination of treatment outcomes—direct toxicity and immunotoxicity—to kill the tumor while exploiting immunotherapy to potentially prevent the recurrence of GBM. The new molecule, a fusion superkine (FSK), contains dual-acting therapeutic cytokines in a single molecule.

“This is the tip of the iceberg,” said Dr. Fisher, the Thelma Newmeyer Corman Endowed Chair in Cancer Research at Massey, director of the VIMM and professor in the Department of Cellular, Molecular and Genetic Medicine. “We’re optimistic that our first trial in , planned for 2026, will show that the IL-24 gene and these therapeutic viruses are effective and safe. And [the FSK] will be the one knocking it out of the ballpark.

‘ALS on a chip’ model reveals altered motor neuron signaling

Using stem cells from patients with ALS (amyotrophic lateral sclerosis), Cedars-Sinai has created a lifelike model of the mysterious and fatal disease that could help identify a cause of the illness as well as effective treatments.

In a study published in the journal Cell Stem Cell, investigators detail how they created “ALS on a chip” and the clues the specialized laboratory chip has already produced about nongenetic causes of the disease, also known as Lou Gehrig’s disease.

The work builds on previous studies where adult cells from ALS patients were reverted into . The cells were then pushed forward to produce motor neurons, which die in the disease, causing progressive loss of the ability to move, speak, eat and breathe.

Gene editing treats smooth muscle disease in preclinical model

Using gene editing in a preclinical model, researchers at UT Southwestern Medical Center blocked the symptoms of a rare smooth muscle disease before they developed. Their findings, published in Circulation, could eventually lead to gene therapies for this and other genetic diseases affecting smooth muscle cells.

“Gene editing has been used in other disease contexts, but its application to inherited vascular diseases, particularly targeting in vivo, is still emerging. Our approach advances the field by demonstrating functional correction in a cell type that’s notoriously difficult to target,” said Eric Olson, Ph.D., Chair and Professor of Molecular Biology and a member of the Harold C. Simmons Comprehensive Cancer Center at UT Southwestern.

Dr. Olson co-led the study with Ning Liu, Ph.D., Professor of Molecular Biology, and first author Qianqian Ding, Ph.D., postdoctoral researcher, both members of the Olson Lab.

Rare Gene Mutation Delays Alzheimer’s by Damping Immune Cell Inflammatory Signaling

Researchers at Weill Cornell Medicine report that a rare gene mutation that delays Alzheimer’s disease does so by damping inflammatory signaling in brain-resident immune cells in a preclinical study. The finding adds to growing evidence that brain inflammation is a major driver of neurodegenerative disorders such as Alzheimer’s—and that it may be a key therapeutic target for these disorders.

In their study “The R136S mutation in the APOE3 gene confers resilience against tau pathology via inhibition of the cGAS-STING-IFN pathway,” in Immunity, the investigators examined the effects of the mutation APOE3-R136S—known as the “Christchurch mutation”—which was recently found to delay hereditary early-onset Alzheimer’s. The scientists showed that the mutation inhibits the cGAS-STING pathway, an innate immune signaling cascade that is abnormally activated in Alzheimer’s and other neurodegenerative diseases. The researchers found that pharmacologically blocking the cGAS-STING pathway with a drug-like inhibitor replicated key protective effects of the mutation in a preclinical model.

“This is an exciting study because it suggests that inhibiting this cGAS-STING pathway could make the brain more resistant to the Alzheimer’s process, even in the face of significant tau accumulation,” said study senior author Li Gan, PhD, the Burton P. and Judith B. Resnick Distinguished Professor in Neurodegenerative Diseases and director of the Helen and Robert Appel Alzheimer’s Disease Research Institute at Weill Cornell Medicine.

“Delete-To-Recruit” — Scientists Discover Simpler Approach to Gene Therapy

Repositioning genes awakens fetal hemoglobin to treat disease. CRISPR editing may change future gene therapy.

Researchers have discovered a promising new approach to gene therapy by reactivating genes that are normally inactive. They achieved this by moving the genes closer to regulatory elements on the DNA known as enhancers. To do so, they used CRISPR-Cas9 technology to cut out the piece of DNA separating the gene from its enhancer. This method could open up new ways to treat genetic diseases. The team demonstrated its potential in treating sickle cell disease and beta-thalassemia, two inherited blood disorders.

In these cases, a malfunctioning gene might be bypassed by reactivating an alternative gene that is usually turned off. This technique, called “delete-to-recruit,” works by altering the distance between genetic elements without introducing new genes or foreign material. The study was conducted by researchers from the Hubrecht Institute (De Laat group), Erasmus MC, and Sanquin, and published in the journal Blood.