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Freely access electrophysiological, morphological, and transcriptomic data measured from thousands of individual mouse & human brain cells via the Allen Cell Types Database:

allen institute

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16,313 次观看 • 1 年前 •via X (Twitter)

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Researchers can freely access the Allen Mouse Brain Common Coordinate Framework (v3), a complete and high-resolution 3D atlas of the mouse brain. Learn more about it at #SfN23

Researchers can freely access the Allen Mouse Brain Common Coordinate Framework (v3), a complete and high-resolution 3D atlas of the mouse brain. Learn more about it at #SfN23

allen institute

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Brain cell communication seen in action. Scientists have captured the millisecond fast process of brain cell communication using advanced imaging. Teams in Berlin and the US used rapid freezing techniques on mouse and human neurons to observe neurotransmitter release and vesicle recycling, revealing key steps and proteins involved. This could help understand brain diseases.

Brain cell communication seen in action. Scientists have captured the millisecond fast process of brain cell communication using advanced imaging. Teams in Berlin and the US used rapid freezing techniques on mouse and human neurons to observe neurotransmitter release and vesicle recycling, revealing key steps and proteins involved. This could help understand brain diseases.

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Beautiful new paper: methods for getting stem-cell derived retinal ganglion cells to integrate into the retina (mouse). Cells were capable of migrating & surviving. #NEIfunded Baranov Lab Levi Todd Mass Eye and Ear Harvard Ophthalmology PNASNews paper:

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Michael F. Chiang, MD

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Cells located in the midline of the embryo play crucial roles in development. These cells often influence cell fate decisions and guide axons to establish bilateral connections. Despite their importance, studying these transient cells and their complex interactions has been challenging. Today, we introduce human midline #assembloids—3D self-organizing cellular clusters derived from stem cells by the functional integration of floor plate #organoids and spinal cord #organoids. We demonstrate that midline assembloids enable cell specification and axon guidance in human neurons. Additionally, we use these assembloids to screen and identify human-enriched factors that control these processes. Work led by the incredible Massimo Onesto & Neal Amin!! More details in the preprint 👇

Cells located in the midline of the embryo play crucial roles in development. These cells often influence cell fate decisions and guide axons to establish bilateral connections. Despite their importance, studying these transient cells and their complex interactions has been challenging. Today, we introduce human midline #assembloids—3D self-organizing cellular clusters derived from stem cells by the functional integration of floor plate #organoids and spinal cord #organoids. We demonstrate that midline assembloids enable cell specification and axon guidance in human neurons. Additionally, we use these assembloids to screen and identify human-enriched factors that control these processes. Work led by the incredible Massimo Onesto & Neal Amin!! More details in the preprint 👇

Sergiu P. Pasca

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This is only 1 Niagara emitter to handle thousands of decals as particles using Data Channels! Significantly lower overhead on the GameThread and only a single component per grid cell. This also adds instancing to the decals which is normally not supported for individual decal components. Working on this as part of data-oriented projectiles that run without Actors, asynchronous collision and supporting multiplayer (incl. client side prediction). Removes a huge amount of overhead from the CPU, more on that soon!

This is only 1 Niagara emitter to handle thousands of decals as particles using Data Channels! Significantly lower overhead on the GameThread and only a single component per grid cell. This also adds instancing to the decals which is normally not supported for individual decal components. Working on this as part of data-oriented projectiles that run without Actors, asynchronous collision and supporting multiplayer (incl. client side prediction). Removes a huge amount of overhead from the CPU, more on that soon!

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New Cell paper from Bergles lab at Johns Hopkins just built the most comprehensive map of brain myelin ever made — every oligodendrocyte, across the entire mouse brain, across the lifespan. The scale: >10 million cells per brain, terabyte-scale 3D lightsheet volumes, registered to the Allen Brain Atlas across 417 regions from 2 months to 2+ years of age. The technical stack: Custom tissue clearing (CUBIC-L + SHIELD + uRIMS with 40% urea) to preserve endogenous fluorescence. 3D Mask R-CNN for instance segmentation — not just semantic, instance — so it can distinguish individual cells within dense clusters at scale via overlapping sliding windows. Vision Transformer to classify newly-formed vs. mature oligodendrocytes using soma morphology. All cross-referenced against Allen ISH transcriptomics and MICrONS serial EM. What they found: Oligodendrocyte density varies 10,000-fold across brain regions. Left-right hemispheres: r=0.99. Sex: no significant difference. Strain: matters. The brain never stops myelinating. New oligodendrocytes are still being generated in 2-year-old mice. Prefrontal cortex L6 shows the fastest rates of new myelination into old age — the circuits for executive function keep rewiring throughout life. After demyelination, L4 sensory cortex is the most resilient — oligodendrocytes survive at higher rates. The hippocampus loses nearly everything and barely recovers. Degree of injury doesn't predict rate of recovery. These are independent axes. The Alzheimer's result is the most surprising: Dense-core plaques dominate in cortex and hippocampus. Diffuse/small-core plaques dominate in white matter fiber tracts. Old assumption: diffuse plaques are "less toxic." The data says the opposite — small plaques in fiber tracts cause more myelin loss per plaque than dense-core plaques in gray matter. Plaque load and oligodendrocyte loss are essentially uncorrelated (ρ=0.22). The damage is plaque-type and location specific, not load-dependent. For MS and AD research: you can't read off white matter injury from gray matter plaque burden. The pathology in fiber tracts is running on different rules. Data: Paper:

New Cell paper from Bergles lab at Johns Hopkins just built the most comprehensive map of brain myelin ever made — every oligodendrocyte, across the entire mouse brain, across the lifespan. The scale: >10 million cells per brain, terabyte-scale 3D lightsheet volumes, registered to the Allen Brain Atlas across 417 regions from 2 months to 2+ years of age. The technical stack: Custom tissue clearing (CUBIC-L + SHIELD + uRIMS with 40% urea) to preserve endogenous fluorescence. 3D Mask R-CNN for instance segmentation — not just semantic, instance — so it can distinguish individual cells within dense clusters at scale via overlapping sliding windows. Vision Transformer to classify newly-formed vs. mature oligodendrocytes using soma morphology. All cross-referenced against Allen ISH transcriptomics and MICrONS serial EM. What they found: Oligodendrocyte density varies 10,000-fold across brain regions. Left-right hemispheres: r=0.99. Sex: no significant difference. Strain: matters. The brain never stops myelinating. New oligodendrocytes are still being generated in 2-year-old mice. Prefrontal cortex L6 shows the fastest rates of new myelination into old age — the circuits for executive function keep rewiring throughout life. After demyelination, L4 sensory cortex is the most resilient — oligodendrocytes survive at higher rates. The hippocampus loses nearly everything and barely recovers. Degree of injury doesn't predict rate of recovery. These are independent axes. The Alzheimer's result is the most surprising: Dense-core plaques dominate in cortex and hippocampus. Diffuse/small-core plaques dominate in white matter fiber tracts. Old assumption: diffuse plaques are "less toxic." The data says the opposite — small plaques in fiber tracts cause more myelin loss per plaque than dense-core plaques in gray matter. Plaque load and oligodendrocyte loss are essentially uncorrelated (ρ=0.22). The damage is plaque-type and location specific, not load-dependent. For MS and AD research: you can't read off white matter injury from gray matter plaque burden. The pathology in fiber tracts is running on different rules. Data: Paper:

Bo Wang

24,777 次观看 • 6 个月前

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AI runs on data. but most of it is stale, outdated, static. what if intelligence was powered by living signals from real human activity? introducing: 𝐳𝐃𝐚𝐭𝐚 - the Data Layer Powering Zentry and The AI Data Economy ⇢

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$🚨 Scientists discover wisdom teeth contain stem cells capable of repairing the heart, brain, and bones. Wisdom teeth contain dental pulp, a soft connective tissue threaded with blood vessels and nerves. Inside that pulp lives a dense population of mesenchymal stem cells, a class of undifferentiated cells that researchers classify as among the most therapeutically valuable biological material a human body produces. These are not ordinary cells maintaining routine tissue. They are blueprint cells, capable of receiving chemical signals from damaged environments and reshaping themselves into whatever the body needs most, neurons, cardiomyocytes, osteoblasts, even hepatic cells under the right conditions. The brain operates under a brutal rule: most of its neurons do not regenerate after damage. A stroke, a traumatic injury, a neurodegenerative disease removes cells the brain cannot replace through normal biological processes. Researchers have spent decades attempting to solve this through synthetic means, engineered cell therapies, growth factor injections, gene editing approaches that cost extraordinary resources and produce inconsistent results. What dental pulp stem cells demonstrated in laboratory conditions is that they can migrate toward neural damage sites, integrate with existing tissue architecture, and begin producing neurons and glial support cells. The mechanism involves neurotrophic factor secretion, essentially the cells releasing signaling proteins that stimulate the surrounding neural environment to repair itself from within. Cardiac muscle operates under a similarly unforgiving rule. After a heart attack, the dead muscle tissue becomes fibrotic scar material. The heart compensates by making surviving muscle work harder, a process that gradually leads to enlargement, weakening, and eventual failure. Dental pulp stem cells introduced into cardiac tissue in multiple studies produced measurable reductions in scar formation and demonstrated the ability to differentiate into functional cardiomyocytes, beating in synchrony with native heart cells. Some studies recorded improved ejection fraction in animal models, the core measurement of how effectively the heart pumps blood. Bone regeneration represents the most clinically advanced application already moving toward human trials. Dental pulp stem cells express high levels of osteogenic markers and respond rapidly to bone morphogenetic proteins, the chemical messengers that trigger skeletal repair. Their application in craniofacial reconstruction, spinal fusion, and long bone defect repair is being studied across multiple institutions simultaneously. What separates these cells from other stem cell sources is the combination of accessibility and biological youth. Bone marrow aspiration requires sedation and produces significant post procedure pain. Umbilical cord blood requires planning around birth. Wisdom teeth emerge between 17 and 25, during peak cellular vitality, and come out during a procedure most people already schedule. The extraction window is permanent. Once the teeth are gone and the pulp degrades, that specific population of young, highly potent cells is irretrievable from that individual. Cryogenic preservation protocols now exist that maintain dental pulp stem cell viability for over two decades. Several countries have commercial dental stem cell banks operating with the same institutional model as cord blood banking, long term frozen storage, indexed against future therapeutic need. The science supporting the value of preservation is no longer speculative. What lags behind is public awareness and clinical infrastructure in markets where this remains obscure. The wider pattern is worth recognizing. Medicine has repeatedly discovered that profound biological tools were present in tissues it previously categorized as vestigial, unnecessary, or inconvenient. The appendix was considered evolutionary junk for over a century before researchers identified its role in gut microbiome preservation. Wisdom teeth carried the same dismissal, a developmental relic from ancestors who needed extra molars for coarse diets, relevant only in their capacity to cause orthodontic problems. The pulp inside them was never junk. It was a repair system the body built during youth and stored in one of the most protected anatomical locations, surrounded by enamel, the hardest substance the human body produces. Evolution rarely wastes that kind of architecture.$

🚨 Scientists discover wisdom teeth contain stem cells capable of repairing the heart, brain, and bones. Wisdom teeth contain dental pulp, a soft connective tissue threaded with blood vessels and nerves. Inside that pulp lives a dense population of mesenchymal stem cells, a class of undifferentiated cells that researchers classify as among the most therapeutically valuable biological material a human body produces. These are not ordinary cells maintaining routine tissue. They are blueprint cells, capable of receiving chemical signals from damaged environments and reshaping themselves into whatever the body needs most, neurons, cardiomyocytes, osteoblasts, even hepatic cells under the right conditions. The brain operates under a brutal rule: most of its neurons do not regenerate after damage. A stroke, a traumatic injury, a neurodegenerative disease removes cells the brain cannot replace through normal biological processes. Researchers have spent decades attempting to solve this through synthetic means, engineered cell therapies, growth factor injections, gene editing approaches that cost extraordinary resources and produce inconsistent results. What dental pulp stem cells demonstrated in laboratory conditions is that they can migrate toward neural damage sites, integrate with existing tissue architecture, and begin producing neurons and glial support cells. The mechanism involves neurotrophic factor secretion, essentially the cells releasing signaling proteins that stimulate the surrounding neural environment to repair itself from within. Cardiac muscle operates under a similarly unforgiving rule. After a heart attack, the dead muscle tissue becomes fibrotic scar material. The heart compensates by making surviving muscle work harder, a process that gradually leads to enlargement, weakening, and eventual failure. Dental pulp stem cells introduced into cardiac tissue in multiple studies produced measurable reductions in scar formation and demonstrated the ability to differentiate into functional cardiomyocytes, beating in synchrony with native heart cells. Some studies recorded improved ejection fraction in animal models, the core measurement of how effectively the heart pumps blood. Bone regeneration represents the most clinically advanced application already moving toward human trials. Dental pulp stem cells express high levels of osteogenic markers and respond rapidly to bone morphogenetic proteins, the chemical messengers that trigger skeletal repair. Their application in craniofacial reconstruction, spinal fusion, and long bone defect repair is being studied across multiple institutions simultaneously. What separates these cells from other stem cell sources is the combination of accessibility and biological youth. Bone marrow aspiration requires sedation and produces significant post procedure pain. Umbilical cord blood requires planning around birth. Wisdom teeth emerge between 17 and 25, during peak cellular vitality, and come out during a procedure most people already schedule. The extraction window is permanent. Once the teeth are gone and the pulp degrades, that specific population of young, highly potent cells is irretrievable from that individual. Cryogenic preservation protocols now exist that maintain dental pulp stem cell viability for over two decades. Several countries have commercial dental stem cell banks operating with the same institutional model as cord blood banking, long term frozen storage, indexed against future therapeutic need. The science supporting the value of preservation is no longer speculative. What lags behind is public awareness and clinical infrastructure in markets where this remains obscure. The wider pattern is worth recognizing. Medicine has repeatedly discovered that profound biological tools were present in tissues it previously categorized as vestigial, unnecessary, or inconvenient. The appendix was considered evolutionary junk for over a century before researchers identified its role in gut microbiome preservation. Wisdom teeth carried the same dismissal, a developmental relic from ancestors who needed extra molars for coarse diets, relevant only in their capacity to cause orthodontic problems. The pulp inside them was never junk. It was a repair system the body built during youth and stored in one of the most protected anatomical locations, surrounded by enamel, the hardest substance the human body produces. Evolution rarely wastes that kind of architecture.

The Curious Tales

24,267 次观看 • 5 个月前