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A groundbreaking data storage technology could preserve an entire human genome in a tiny 5D memory crystal. Developed by researchers at the University of Southampton, this innovation has the potential to last billions of years, offering an unprecedented solution for long-term data preservation.

Beyond human genetics, the technology could safeguard the genomes of endangered species. If future science enables species revival, these stored genetic blueprints might help restore lost biodiversity. The crystals could also serve as an indestructible archive of human knowledge.

Unlike conventional storage methods —hard drives, magnetic tapes, or optical discs—the 5D crystal doesn’t degrade over time. Standard formats fail within decades, but this breakthrough resists extreme conditions without data loss. It could endure for billions of years, even in the harshest environments.

There’s a window of time in our lives we’ve all passed through yet still know so little about: early gestation. Researchers have found a pair of genetic deletions associated with schizophrenia that likely occur in that formative period.

The discovery comes from a team of researchers led by Harvard Medical School clinician-scientist Eduardo Maury, who combed through genetic data from blood samples of nearly 25,000 people with or without schizophrenia.

While the two genetic alterations need further validation, the findings strengthen an emerging idea that the seeds of schizophrenia aren’t always inherited, yet still may be acquired long before someone meets the world.

Alopecia refers to hair loss and can affect the scalp, eyebrows, eyelashes, and other areas of the body. There are different types of alopecia including androgenetic alopecia, alopecia areata, anagen effluvium, and frontal fibrosing alopecia (FFA). Each form of disease refers to where and how hair is lost. This type of categorization helps physicians best diagnose and treat patients. Frontal fibrosing alopecia was first recognized in the early 1990s and still puzzles scientists and physicians. It is characterized by progressive loss with hair follicles becoming inflamed and destroyed. Eyebrow thinning is also a common symptom along with skin redness and scaling, and wrinkling.

Unfortunately, the cause of FFA is unknown and is a type of scarring hair loss, which means that the hair cannot grow back. This particularly distressing condition is thought to be the result of an autoimmune disorder. Many scientists believe FFA is caused by hormonal imbalances or genetic predispositions. Scientists are currently trying to find ways to cure or permanently treat FFA. Treatment options to date include topical corticosteroids, oral medication, light therapy, and hair transplantation. However, all of these treatments work to relieve symptoms, delay hair loss, or replace hair loss. Since FFA is a chronic condition, symptoms can progress over time and with early intervention, patients can significantly delay hair loss. The lack of sufficient treatment is still a concern, and many researchers are investigating how to overcome this disease and avoid hair loss.

A recent paper in JAMA Dermatology, by Dr. Christos Tziotzios and others, reported a change in two areas of the human genome that can influence alopecia risk. This is a major advance in the field of alopecia and can be used to enhance treatment. Tziotzios is a Consultant Dermatologist and Senior Lecturer at St. John’s Institute of Dermatology in the United Kingdom (UK). He specializes in general dermatology and hair and scalp disorders including FFA in both biological males and females.

Science and Technology: Gene Therapy apparently Cure Blindness in Children.

S eye, very early in life, to treat a severe form of the condition.‘.


An experimental trial of gene therapy has helped four toddlers — born with one of the most severe forms of childhood blindness — gain “life-changing improvements” to their sight, according to doctors at Moorfields Eye Hospital in London.

The rare genetic condition means the babies’ vision deteriorated very rapidly from birth.

Very excellent.


Arc Institute researchers have developed a machine learning model called Evo 2 that is trained on the DNA of over 100,000 species across the entire tree of life. Its deep understanding of biological code means that Evo 2 can identify patterns in gene sequences across disparate organisms that experimental researchers would need years to uncover. The model can accurately identify disease-causing mutations in human genes and is capable of designing new genomes that are as long as the genomes of simple bacteria.

Evo 2’s developers—made up of scientists from Arc Institute and NVIDIA, convening collaborators across Stanford University, UC Berkeley, and UC San Francisco—will post details about the model as a preprint on February 19, 2025, accompanied by a user-friendly interface called Evo Designer. The Evo 2 code is publicly accessible from Arc’s GitHub, and is also integrated into the NVIDIA BioNeMo framework, as part of a collaboration between Arc Institute and NVIDIA to accelerate scientific research. Arc Institute also worked with AI research lab Goodfire to develop a mechanistic interpretability visualizer that uncovers the key biological features and patterns the model learns to recognize in genomic sequences. The Evo team is sharing its training data, training and inference code, and model weights to release the largest-scale, fully open source AI model to date.

Building on its predecessor Evo 1, which was trained entirely on single-cell genomes, Evo 2 is the largest artificial intelligence model in biology to date, trained on over 9.3 trillion nucleotides—the building blocks that make up DNA or RNA—from over 128,000 whole genomes as well as metagenomic data. In addition to an expanded collection of bacterial, archaeal, and phage genomes, Evo 2 includes information from humans, plants, and other single-celled and multi-cellular species in the eukaryotic domain of life.

Unraveling the Genetic Risk of Cancer

Thousands of tiny changes in the DNA sequence of the human genome have been linked to an increased risk of cancer. However, until now, it has been unclear which of these changes directly contribute to the uncontrolled cell growth that defines the disease and which are simply coincidences or minor players.

Stanford researchers conducted the first large-scale analysis of these inherited genetic changes, known as single nucleotide variants. Their study identified fewer than 400 variants that play a key role in triggering and sustaining cancer growth. These variants influence several critical biological pathways, including those that control DNA repair, energy production, and how cells interact with their microenvironment.

New in JNeurosci: Researchers identified a new subset of neurons in mice that morphine may interact with to influence behavior. This neuron population could be a promising new opioid addiction treatment target.

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Opioid use disorder constitutes a major health and economic burden, but our limited understanding of the underlying neurobiology impedes better interventions. Alteration in the activity and output of dopamine (DA) neurons in the ventral tegmental area (VTA) contributes to drug effects, but the mechanisms underlying these changes remain relatively unexplored. We used translating ribosome affinity purification and RNA sequencing to identify gene expression changes in mouse VTA DA neurons following chronic morphine exposure. We found that expression of the neuropeptide neuromedin S (Nms) is robustly increased in VTA DA neurons by morphine. Using an NMS-iCre driver line, we confirmed that a subset of VTA neurons express NMS and that chemogenetic modulation of VTA NMS neuron activity altered morphine responses in male and female mice. Specifically, VTA NMS neuronal activation promoted morphine locomotor activity while inhibition reduced morphine locomotor activity and conditioned place preference (CPP). Interestingly, these effects appear specific to morphine, as modulation of VTA NMS activity did not affect cocaine behaviors, consistent with our data that cocaine administration does not increase VTA Nms expression. Chemogenetic manipulation of VTA neurons that express glucagon-like peptide, a transcript also robustly increased in VTA DA neurons by morphine, does not alter morphine-elicited behavior, further highlighting the functional relevance of VTA NMS-expressing neurons. Together, our current data suggest that NMS-expressing neurons represent a novel subset of VTA neurons that may be functionally relevant for morphine responses and support the utility of cell type-specific analyses like TRAP to identify neuronal adaptations underlying substance use disorder.

Significance Statement The opioid epidemic remains prevalent in the U.S., with more than 70% of overdose deaths caused by opioids. The ventral tegmental area (VTA) is responsible for regulating reward behavior. Although drugs of abuse can alter VTA dopaminergic neuron function, the underlying mechanisms have yet to be fully explored. This is partially due to the cellular heterogeneity of the VTA. Here, we identify a novel subset of VTA neurons that express the neuropeptide neuromedin S (NMS). Nms expression is robustly increased by morphine and alteration of VTA NMS neuronal activity is sufficient to alter morphine-elicited behaviors. Our findings are the first to implicate NMS-expressing neurons in drug behavior and thereby improve our understanding of opioid-induced adaptations in the VTA.

Several multi-cancer GWAS loci within the region encoding telomerase reverse transcriptase (TERT) have been identified. Here, the authors explore the locus within TERT intron 4, link it with a variable number tandem repeat (VNTR), and investigate its biological significance and role in cancer.

🔍 Overview: Join Robert Plomin and me as we dive deep into the fascinating world of behavioural genetics, exploring how our DNA shapes who we are, the power of environment, and whether we can rewrite our genetic destiny.

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PayPal: https://www.paypal.com/paypalme/samuehttps://www.blockchain.com/explorer/a… 🗣️ Highlights [Highlight 1]: How Does Genetics Shape Who We Are? [Highlight 2]: What Role Does the Environment Truly Play in Defining Us? [Highlight 3]: Are We Hardwired by Our DNA, or Can We Rewrite Our Destiny? 🕒 Timestamps 0:00 — Introduction 1:57 — Robert Plomin, Philosophy and Psychology 4:12 — Why Behavioural Genetics? 8:21 — Publishing Blueprint 14:51 — Heritability 30:15 — The Basics of DNA 34:34 — Genetic Variances and Binary Myths 41:21 — Labels and Certificates 45:33 — Nonshared Environments and The Nature of Nurture 1:00:51 — Self-Selecting Within Environments 1:07:04 — Group Difference and Heritability 1:13:03 — Academic Success: DNA vs. Schooling 1:21:17 — Ethical Considerations 1:27:01 — Moral Responsibility and Accountability 1:31:23 — The Future of Genetics 1:42:38 — Genetic Trajectories and Random Events 1:45:17 — The DNA Revolution 1:48:21 — Closing Remarks 📚 Episode Resources (affiliate links where possible — thanks!) Blueprint: How DNA Makes Us Who We Are by Robert Plomin: https://amzn.to/3T9htYp King’s College London: https://www.kcl.ac.uk/people/robert-p… Common Disorders are Quantitative Traits by Robert Plomin: https://pubmed.ncbi.nlm.nih.gov/19859… Gattaca (1997): https://www.imdb.com/title/tt0119177/ 🌐 Connect Linktree: https://linktr.ee/samueldevis89 Substack: https://thesocraticsessions.substack… Twitter: / samueldevis89 Facebook Page: / thesocraticsessions Instagram: / samueldevis89 Goodreads: / samuel-devis Bluesky: https://bsky.app/profile/samueldevis8… Threads: https://www.threads.net/@samueldevis89 LinkedIn Page: / thesocraticsessions 🎧 Subscribe 📺 YouTube: / @samueldevis89 Rumble: https://rumble.com/c/SamuelDevis89 Apple Podcasts: https://podcasts.apple.com/us/podcast… Spotify: https://open.spotify.com/show/6lOdYbN… Audible: https://www.audible.co.uk/pd/The-Socr… Amazon Music: https://music.amazon.co.uk/podcasts/3… Other Podcast Platforms: https://podcasters.spotify.com/pod/sh… 📷 Gear (affiliate links — thanks!) Camera (Sony A6400): https://amzn.to/46jehNn Lens (Sigma 16mm): https://amzn.to/47DfiRn Audio Interface (Focusrite Scarlett 4i4): https://amzn.to/47lJzEP Microphone Amplifier (Cloudlifter CL-1): https://amzn.to/3uou7Jq Mic (RØDE PodMic): https://amzn.to/3sJFUBE Lights (Elgato Key Light Air): https://amzn.to/3TZMgYX Colour Back Lighting (Govee LED Floor Lamp): https://amzn.to/47EGSOf Recording Software (Riverside. FM): https://www.tinyurl.com/riversidesam89 👍 Support: Like, subscribe, and share to fuel the quest for understanding. 🔔 Stay Tuned: Tap the bell for instant notifications. 📣 Join the Talk: Share your thoughts using #TheSocraticSessions. 🚀 Thanks for Tuning In! Let’s keep the conversation going. #genetics #nature #nurture #dna #heritability #genome #biology #philosophy.
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🗣️ Highlights.
[Highlight 1]: How Does Genetics Shape Who We Are?
[Highlight 2]: What Role Does the Environment Truly Play in Defining Us?
[Highlight 3]: Are We Hardwired by Our DNA, or Can We Rewrite Our Destiny?

🕒 Timestamps.

A cancer therapy that uses genetically engineered immune cells, called CAR T-cells, has kept a person free of a potentially fatal nerve tumour for a record-breaking 18 years.⁠ ⁠ “This is, to my knowledge, the longest-lasting complete remission in a patient who received CAR T-cell therapy,” says Karin Straathof at University College London, who wasn’t involved in the treatment. “This patient is cured,” she says.⁠ ⁠ Doctors use CAR T-cell therapy to treat some kinds of blood cancer, like leukaemia. To do this, they collect a sample of T-cells, which form part of the immune system, from a patient’s blood and genetically engineer them to target and kill cancer cells. They then infuse the modified cells back into the body. In 2022, a follow-up study found that this approach had put two people with leukaemia into remission for around 11 years, a record at the time.⁠ ⁠