How Did Humans Develop Sharp Vision? Lab-Grown Retinas Show Likely Answer

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Image Credit: Scientific Frontline

Scientific Frontline: Extended "At a Glance" Summary: Retina Organoids & Human Vision

The Core Concept: Retina organoids are lab-grown, three-dimensional clusters of retinal tissue derived from fetal cells that replicate the developmental processes of the human eye in a controlled environment.

Key Distinction/Mechanism: Unlike previous models which suggested blue cone cells physically migrated out of the central retina (foveola), these organoids revealed that cells undergo a conversion process. The mechanism is two-fold: retinoic acid (a vitamin A derivative) breaks down to limit the initial creation of blue cones, and thyroid hormones subsequently signal the remaining blue cones to transform into red and green cones, establishing the specialized pattern required for sharp daytime vision.

Origin/History: The findings were published in the Proceedings of the National Academy of Sciences around February 18, 2026. This research challenges a prevailing 30-year-old biological theory regarding how the eye distributes light-sensing cells during development.

Major Frameworks/Components:

• Organoid Technology: The cultivation of "mini-retinas" in petri dishes to observe long-term developmental timelines.
• The Foveola: The specific central region of the retina responsible for 50% of visual perception and high-acuity vision.
• Cell Fate Specification: The biological programming that determines whether a photoreceptor becomes a blue, green, or red cone.
• Hormonal Signaling: The specific interplay between retinoic acid and thyroid hormones in dictating cell identity.

Disrupting pathogenic cell states to combat pulmonary fibrosis

Image Credit: Scientific Frontline

Scientific Frontline: "At a Glance" Summary

• Main Discovery: Inhibition of the epigenetic co-activators p300/CBP prevents alveolar type 2 (AT2) cells from becoming trapped in a pathogenic "alveolar transitional cell state" (ATCS), thereby blocking the progression of idiopathic pulmonary fibrosis (IPF).
• Methodology: Researchers utilized a phenotypic drug screen of 264 compounds on human iPS cell-derived models and validated efficacy using a bleomycin-induced mouse lung injury model and a telomere-driven senescence model.
• Key Data: The p300/CBP inhibitor CBP30 significantly decreased fibrotic gene expression and myofibroblast activation, while single-cell profiling identified CD54 (ICAM1) as a distinct surface marker for isolating pathogenic ATCS cells.
• Significance: This study demonstrates that the accumulation of ATCS is a reversible, epigenetically driven process central to fibrosis, identifying a novel therapeutic target for a disease characterized by irreversible tissue scarring.
• Future Application: Development of targeted p300/CBP inhibitors as a new class of antifibrotic drugs for treating idiopathic pulmonary fibrosis and potentially other interstitial lung diseases.
• Branch of Science: Regenerative Medicine / Epigenetics.
• Additional Detail: Transcriptomic analysis confirmed that the iPS cell-derived ATCS (iATCs) generated in the study closely match the pathological cell states found in the lungs of human IPF patients.

Paralysis treatment heals lab-grown human spinal cord organoids

Fluorescent micrographs showing increased neurite outgrowth from a human spinal cord organoid treated with fast-moving “dancing molecules” (left) compared to one treated with slow-moving molecules (right) containing the same bioactive signals
Image Credit: Samuel I. Stupp/Northwestern University

Scientific Frontline: Extended "At a Glance" Summary

The Core Concept: Lab-grown human spinal cord organoids are miniature, three-dimensional tissue models derived from stem cells that mimic the complex structure and function of the human spinal cord to simulate injuries and test regenerative treatments.

Key Distinction/Mechanism: Unlike previous models, these organoids incorporate microglia—the central nervous system's immune cells—allowing researchers to accurately replicate the inflammatory response and glial scarring seen in human spinal cord injuries. The "dancing molecules" therapy creates a nanofiber scaffold where rapidly moving molecules effectively engage cellular receptors to trigger neurite growth and reverse paralysis, a mechanism significantly more effective than therapies using static molecules.

Major Frameworks/Components:

• Induced Pluripotent Stem Cells (iPSCs): The source material for growing the organoids, allowing for patient-specific tissue generation.
• Supramolecular Therapeutic Peptides (STPs): The chemical basis of the "dancing molecules" that assemble into nanofibers.
• Microglia Integration: The inclusion of immune cells to create a "pseudo-organ" that mimics natural inflammatory responses.
• Glial Scarring: A physical barrier to nerve regeneration that the therapy successfully diminished in trials.

Branch of Science: Regenerative Medicine, Nanotechnology, Neuroscience, and Bioengineering.

Future Application: The technology paves the way for personalized medicine, where a patient's own stem cells could be used to grow implantable tissues that avoid immune rejection. It also offers a platform to test treatments for chronic, long-term spinal cord injuries and other neurodegenerative conditions.

Why It Matters: This advancement bridges the gap between animal studies and clinical trials, providing a highly accurate human model for spinal cord injury. It validates a promising therapy that has earned Orphan Drug Designation from the FDA, offering renewed hope for restoring function in paralyzed patients.

Aggressive brain tumors build protective “sugar shield” to survive extreme stress

Mattias Belting and Anna Bång Rudenstam.
Photo Credit: Tove Smeds

Scientific Frontline: "At a Glance" Summary

• Main Discovery: Aggressive brain tumors, specifically glioblastoma and central nervous system metastases, construct a protective surface layer rich in chondroitin sulfate to shield themselves from toxic lipids and prevent ferroptosis (a form of cell death caused by lipid oxidation).
• Methodology: Researchers analyzed tumor cells isolated directly from patient surgeries and utilized 3D organoid models to replicate the tumor environment; they then experimentally disrupted the formation of the sugar shield while simultaneously blocking the cells' ability to store lipids in droplets.
• Key Data: The study identified two cooperative defense mechanisms: the external chondroitin sulfate sugar shield (acting as a filter) and internal lipid droplets (acting as storage buffers); simultaneously disabling both defenses caused rapid tumor cell collapse and death via ferroptosis.
• Significance: This finding reveals a previously unrecognized metabolic survival strategy that allows cancer cells to adapt to the brain's hostile environment (characterized by oxidative stress and low pH), fundamentally changing the understanding of brain tumor resilience.
• Future Application: The discovery points toward a novel therapeutic strategy that combines agents to strip the sugar shield with inhibitors of lipid storage, potentially sensitizing aggressive tumors to ferroptosis-inducing treatments.
• Branch of Science: Oncology and Cell Biology
• Additional Detail: The same protective sugar shield mechanism was observed in brain metastases originating from malignant melanoma, lung cancer, and kidney cancer, suggesting a common adaptive trait for tumors invading the central nervous system.

Misplaced Neurons Reveal the Brain’s Adaptability

Image Credit: Scientific Frontline / AI generated (Gemini)

Scientific Frontline: "At a Glance" Summary

• Main Discovery: Neurons positioned in the wrong location, known as heterotopias, can successfully integrate into brain circuits and take over the functional role of the normal cerebral cortex, defying the assumption that precise anatomical placement is required for function.
• Methodology: Researchers utilized a mouse model with induced heterotopias and performed functional mapping during a sensory task requiring the distinction of whiskers; they employed targeted deactivation to isolate the contributions of normal versus misplaced neurons.
• Key Data: Mice continued to perform sensory tasks normally when the healthy cortex was deactivated; however, the specific inhibition of the misplaced neuronal clusters resulted in immediate and complete failure of the task.
• Significance: This study fundamentally alters the understanding of brain plasticity, demonstrating that cellular identity and connectivity can override spatial positioning to maintain neurological function.
• Future Application: These findings validate the potential of regenerative therapies, such as neuronal grafts and brain organoids, suggesting they can be effective treatments without needing to perfectly replicate natural brain architecture.
• Branch of Science: Neuroscience (Neurodevelopment and Plasticity).
• Additional Detail: Analysis revealed that these stray neurons formed neural circuits almost identical to those in the healthy cortex, establishing correct connections with both the rest of the brain and the spinal cord.

What Is: Organoid

Organoids: The Science and Ethics of Mini-Organs
Image Credit: Scientific Frontline / AI generated

The "At a Glance" Summary

• Defining the Architecture: Unlike traditional cell cultures, organoids are 3D structures grown from pluripotent stem cells (iPSCs) or adult stem cells. They rely on the cells' intrinsic ability to self-organize, creating complex structures that mimic the lineage and spatial arrangement of an in vivo organ.
• The "Avatar" in the Lab: Organoids allow for Personalized Medicine. By growing an organoid from a specific patient's cells, researchers can test drug responses on a "digital twin" of that patient’s tumor or tissue, eliminating the guesswork of trial-and-error prescriptions.
• Bridge to Clinical Trials: Organoids serve as a critical bridge between the Petri dish and human clinical trials, potentially reducing the failure rate of new drugs and decreasing the reliance on animal testing models which often fail to predict human reactions.
• The Ethical Frontier: As cerebral organoids (mini-brains) become more complex, exhibiting brain waves similar to preterm infants, science faces a profound question: At what point does biological complexity become sentience?

Restoring the healthy form of a protein could revive blood vessel growth in premature infants’ lungs

A blood vessel organoid.
Video Credit: Yunpei Zhang and Enbo Zhu, Mingxia Gu Lab

A UCLA-led research team has discovered a molecular switch that determines whether tiny blood vessels in premature infants’ lungs can regenerate after injury. A failure of this repair process is a hallmark of bronchopulmonary dysplasia, or BPD, a serious lung disease that affects babies born very early. It arises from a combination of premature birth, inflammation or infection, and exposure to the high levels of oxygen and breathing support that are necessary to keep these infants alive during a critical period of lung development.

The researchers found that in BPD, the blood vessel cells in the lungs begin producing a shortened, nonfunctional isoform — a version of a protein — called NTRK2, which has been extensively studied in the nervous system but not in the pulmonary vasculature. When this shortened isoform dominates, the lung cannot rebuild the delicate network of tiny blood vessels needed for healthy breathing.

The Quest for the Synthetic Synapse

Spike Timing" difference (Biology vs. Silicon)
Image Credit: Scientific Frontline

The modern AI revolution is built on a paradox: it is incredibly smart, but thermodynamically reckless. A large language model requires megawatts of power to function, whereas the human brain—which allows you to drive a car, debate philosophy, and regulate a heartbeat simultaneously—runs on roughly 20 watts, the equivalent of a dim lightbulb.

To close this gap, science is moving away from the "Von Neumann" architecture (where memory and processing are separate) toward Neuromorphic Computing—chips that mimic the physical structure of the brain. This report analyzes how close we are to building a "synthetic synapse."

Reproduced human neural circuits show the crucial role of the thalamus in shaping the cortical circuit

Assembloid [3D fluorescent staining] Axons in the thalamus (pink) extended toward the cortex, while those in the cortex (green) extended toward the thalamus at 14 days post-fusion.
Image Credit: Fumitaka Osakada

A Japanese research team has successfully reproduced the human neural circuit in vitro using multi-region miniature organs known as assembloids, which are derived from induced pluripotent stem (iPS) cells. With this circuit, the team demonstrated that the thalamus plays a crucial role in shaping cell type-specific neural circuits in the human cerebral cortex.

These findings were published in the journal Proceedings of the National Academy of Sciences of the United States of America.

Our brain’s cerebral cortex contains various types of neurons, and effective communication among these neurons and other brain regions is crucial for activating functions like perception and cognition.

Patients with neurodevelopmental disorders, such as autism spectrum disorder (ASD), exhibit disruptions in the structure and function of neural circuits in the cerebral cortex. Therefore, understanding the principles of these circuits is essential to uncovering the causes of these disorders and developing new medications.

Researchers build bone marrow model entirely from human cells

Scanning electron microscopy image of the engineered 3D bone marrow tissue colonized with human blood cells (red).
Image Credit: Andrés García-García, University of Basel, Department of Biomedicine

Our body’s “blood factory” consists of specialized tissue made up of bone cells, blood vessels, nerves and other cell types. Now, researchers have succeeded for the first time in recreating this cellular complexity in the laboratory using only human cells. The novel system could reduce the need for animal experiments for many applications.

The bone marrow usually works quietly in the background. It only comes into focus when something goes wrong, such as in blood cancers. In these cases, understanding exactly how blood production in our body works, and how this process fails, becomes critical. 

Typically, bone marrow research relies heavily on animal models and oversimplified cell cultures in the laboratory. Now, researchers from the Department of Biomedicine at the University of Basel and University Hospital Basel have developed a realistic model of bone marrow engineered entirely from human cells. This model may become a valuable tool not only for blood cancer research, but also for drug testing and potentially for personalized therapies, as reported by a team of researchers led by Professor Ivan Martin and Dr Andrés García-García in the journal Cell Stem Cell. 

A cellular protein, FGD3, boosts breast cancer chemotherapy, immunotherapy

The research team included, front row, from left: graduate student Junyao Zhu, biochemistry professor David Shapiro, and senior researcher Chengiian Mao; back row, from left: graduate students Abigail Spaulding, Xinyi Dai and Qianjin Jiang.
Photo Credit: Fred Zwicky

A naturally occurring protein that tends to be expressed at higher levels in breast cancer cells boosts the effectiveness of some anticancer agents, including doxorubicin, one of the most widely used chemotherapies, and a preclinical drug known as ErSO, researchers report. The protein, FGD3, contributes to the rupture of cancer cells disrupted by these drugs, boosting their effectiveness and enhancing anticancer immunotherapies.

The new findings were the happy result of experiments involving ErSO, an experimental drug that killed 95-100% of estrogen-receptor-positive breast cancer cells in a mouse model of the disease. ErSO upregulates a cellular pathway that normally protects cancer cells from stress, said University of Illinois Urbana-Champaign biochemistry professor David Shapiro, who led the new work with Illinois graduate student Junyao Zhu. But when that protective pathway is ramped up, the system goes awry.

Did Lead Limit Brain and Language Development in Neanderthals and Other Extinct Hominids?

UC San Diego researchers have found high levels of lead in the teeth of both Neanderthals (left) and modern humans (right). However, a gene mutation may have protected modern human brains, allowing language to flourish.
Photo Credit: Kyle Dykes/UC San Diego Health Sciences

Ancient human relatives were exposed to lead up to two million years ago, according to a new study. However, a gene mutation may have protected modern human brains, allowing language to flourish.

What set the modern human brain apart from our now extinct relatives like Neanderthals? A new study by University of California San Diego School of Medicine and an international team of researchers reveals that ancient hominids — including early humans and great apes — were exposed to lead earlier than previously thought, up to two million years before modern humans began mining the metal. This exposure may have shaped the evolution of hominid brains, limiting language and social development in all but modern humans due to a protective genetic variant that only we carry. The study was published in Science Advances.

The researchers analyzed fossilized teeth from 51 hominids across Africa, Asia and Europe, including modern and archaic humans such as Neanderthals, ancient human ancestors like Australopithecus africanus, and extinct great apes such as Gigantopithecus blacki.

Brain inflammation treatment could be ally in fight against dementia

Samira Aghlara-Fotovat
Photo Credit: Jeff Fitlow/Rice University

Scientists from Rice University and Houston Methodist have developed a new way to reduce inflammation in the brain, a discovery that could help fight diseases such as Alzheimer’s and Parkinson’s.

The team created “AstroCapsules,” small hydrogel capsules that enclose human astrocytes ⎯ star-shaped brain cells that support healthy nervous system function. Inside the capsules, the cells were engineered to release interleukin-1 receptor antagonist, an anti-inflammatory protein. Tests in human brain organoids and mouse models showed the treatment lowered neuroinflammation and resisted immune rejection.

Rice bioengineer Omid Veiseh, whose lab studies how to design biomaterials that work with the immune system, is co-corresponding author on the paper published in Biomaterials.

“Encapsulating cells in a way that shields them from immune attack has been a central challenge in the field,” said Veiseh, professor of bioengineering at Rice, Cancer Prevention and Research Institute of Texas Scholar and director of the Rice Biotech Launch Pad. “In our lab, we have been working on biomaterials for many years, and this project was an opportunity to draw from that experience to address the uniquely complex immune environment of the brain. Our hope is that this work will help move cell therapies closer to becoming real treatment options for patients with neurodegenerative disease.”

Scientists discover potential treatment approaches for polycystic kidney disease

cientists would like to know how cysts form in polycystic kidney disease (PKD). Here, they compared two 3-D mini-kidney models. On the left, a model shows a mini kidney with a gene mutation that causes cysts to form. On the right, researchers used gene editing to correct a gene mutation, preventing the development of cysts.
Image Credit: Vishy, et al., Cell Stem Cell 2024

Researchers have shown that dangerous cysts, which form over time in polycystic kidney disease (PKD), can be prevented by a single normal copy of a defective gene. This means the potential exists that scientists could one day tailor a gene therapy to treat the disease. They also discovered that a type of drug, known as a glycoside, can sidestep the effects of the defective gene in PKD. The discoveries could set the stage for new therapeutic approaches to treating PKD, which affects millions worldwide. The study, partially funded by the National Institutes of Health (NIH), is published in Cell Stem Cell.

Scientists used gene editing and 3-D human cell models known as organoids to study the genetics of PKD, which is a life-threatening, inherited kidney disorder in which a gene defect causes microscopic tubes in the kidneys to expand like water balloons, forming cysts over decades. The cysts can crowd out healthy tissue, leading to kidney function problems and kidney failure. Most people with PKD are born with one healthy gene copy and one defective gene copy in their cells.

“Human PKD has been so difficult to study because cysts take years and decades to form,” said senior study author Benjamin Freedman, Ph.D., at the University of Washington, Seattle. “This new platform finally gives us a model to study the genetics of the disease and hopefully start to provide answers to the millions affected by this disease.”

Not unique to humans but uniquely human: researchers identify factor involved in brain expansion in humans

A microscopy image of a human brain organoid.
Image Credit: © Janine Hoffmann

What makes us human? According to neurobiologists it is our neocortex. This outer layer of the brain is rich in neurons and lets us do abstract thinking, create art, and speak complex languages. An international team led by Dr. Mareike Albert at the Center for Regenerative Therapies Dresden (CRTD) of TUD Dresden University of Technology has identified a new factor that might have contributed to neocortex expansion in humans. The results were published in the EMBO Journal.

The neocortex is the characteristic folded outer layer of the brain that resembles a walnut. It is responsible for higher cognitive functions such as abstract thinking, art, and language. “The neocortex is the most recently evolved part of the brain,” says Dr. Mareike Albert, research group leader at the CRTD. “All mammals have a neocortex, but it varies in size and complexity. Human and primate neocortices have folds while, for example, mice have a completely smooth neocortex, without any creases.”

The folds characteristic of the human brain increases the surface area of the neocortex. The human neocortex has a greater number of neurons that support complex cognitive functions.

The molecular mechanisms driving neocortex evolution are still largely unknown. “Which genes are responsible for inter-species differences in neocortex size? What factors have contributed to brain expansion in humans? Answering these questions is crucial to understanding human brain development and potentially addressing mental health disorders,” explains Dr. Albert.

Human stem cells coaxed to mimic the very early central nervous system

Jianping Fu, Ph.D., Professor of Mechanical Engineering at the University of Michigan and the corresponding author of the paper being published at Nature discusses his team’s work in their lab with Jeyoon Bok, Ph.D. candidate at the Department of Mechanical Engineering.
Photo Credit: Marcin Szczepanski, Michigan Engineering

The first stem cell culture method that produces a full model of the early stages of the human central nervous system has been developed by a team of engineers and biologists at the University of Michigan, the Weizmann Institute of Science, and the University of Pennsylvania.

“Models like this will open doors for fundamental research to understand early development of the human central nervous system and how it could go wrong in different disorders,” said Jianping Fu, U-M professor of mechanical engineering and corresponding author of the study in Nature.

The system is an example of a 3D human organoid—stem cell cultures that reflect key structural and functional properties of human organ systems but are partial or otherwise imperfect copies.

“We try to understand not only the basic biology of human brain development, but also diseases—why we have brain-related diseases, their pathology, and how we can come up with effective strategies to treat them,” said Guo-Li Ming, who along with Hongjun Song, both Perelman Professors of Neuroscience at UPenn and co-authors of the study, developed protocols for growing and guiding the cells and characterized the structural and cellular characteristics of the model.

New treatment for deadly uterine cancer

left to right, Dr Asmerom Sengal, Professor Pamela Pollock.
Photo Credit: Courtesy of Queensland University of Technology

QUT scientists have discovered a promising new therapy for a deadly type of endometrial cancer that has a poor prognosis if the cancer spreads or returns after initial treatment, a plight that affects 15-20 per cent of endometrial cancer patients.

• Testing of new drug inhibited uterine tumor cell growth in lab and mice models

• The drug blocks the receptor of the growth factor in tumors that is associated with a low survival rate

• The inhibitor also reduced the tumors blood vessel formation

Dr Asmerom Sengal and Associate Professor Pamela Pollock from QUT’s School of Biomedical Sciences, published their research in Nature Precision Oncology with a recommendation that the strength of their findings indicated they should proceed to patient trials.

Dr Asmerom said endometrial cancer confined within the uterus could be cured with surgery however, if it had spread to the abdomen and other organs patients had limited treatment options.

“Previously, we found women with endometrial cancer who have an incorrect growth factor receptor called fibroblast growth factor receptor 2c (FGFR2c) on the tumor cell surface have a poor survival rate,” Dr Asmerom said.

Cancer research: Metabolite drives tumor development

Tumor organoids (green/blue) are used as a model to study the metabolic changes in liver cell cancer.
 Image Credit: Dr. Sandro Nuciforo, Department of Biomedicine, University of Basel

Cancer cells are chameleons. They completely change their metabolism to grow continuously. University of Basel scientists have discovered that high levels of the amino acid arginine drive metabolic reprogramming to promote tumor growth. This study suggests new avenues to improve liver cancer treatment.

The liver is a vital organ with many important functions in the body. It metabolizes nutrients, stores energy, regulates the blood sugar level and plays a crucial role in detoxifying and removing harmful components and drugs. Liver cancer is one of the world’s most lethal types of cancer. Conditions that cause liver cancer include obesity, excessive alcohol consumption and hepatitis C infection. Early diagnosis and appropriate therapeutic strategies are crucial for improving treatments in liver cancer.

Cancer as a metabolic disease

In the past decade, scientists have made much progress in understanding the multiple facets of cancer. Historically, it has long been viewed as a disorder in cell proliferation. However, there is growing evidence that cancer is a metabolic disease. In other words, cancer arises when cells rewire their metabolism to allow uncontrolled cell proliferation. How do cells change their metabolism and how does this change in turn lead to tumorigenicity? With their new study in “Cell”, researchers led by Professor Michael N. Hall at the Biozentrum, University of Basel, have discovered a key driver of metabolic rewiring in liver cancer cells.

Fine-tuning 3D lab-grown mini tumors to help predict how patients respond to cancer therapies

The improved process allows researchers to use an advanced imaging method to study and analyze individual organoids in great detail.
Image Credit: Soragni Lab.

Scientists from the UCLA Jonsson Comprehensive Cancer Center have developed a new method to bio-print miniature tumor organoids that are designed to mimic the function and architecture of real tumors. The improved process allows researchers to use an advanced imaging method to study and analyze individual organoids in great detail, which can help researchers identify personalized treatments for people with rare or hard-to-treat cancers.

The method is described in the journal Nature Communications.

“Tumor organoids have become fundamental tools to investigate tumor biology and highlight drug sensitivities of individual patients,” said Alice Soragni, PhD, an assistant professor in the department of Orthopedic Surgery at the David Geffen School of Medicine at UCLA and member of the UCLA Jonsson Comprehensive Cancer Center. “However, we still need better ways to anticipate if resistance could be arising in a small population of cells, which we may not detect using conventional screening approaches. This is truly important, particularly as organoid-based drug predictions are starting to be leveraged clinically.”

Brain research with organoids

Section of an electroporated brain organoid of a common marmoset. Green: electroporated cells that glow green due to the green fluorescent protein; magenta: neurons; gray: nuclei.
Photo Credit: Lidiia Tynianskaia

Scientists at the German Primate Center develop effective method to genetically modify brain organoids

Primates are among the most intelligent creatures with distinct cognitive abilities. Their brains are relatively large in relation to their body stature and have a complex structure. However, how the brain has developed over the course of evolution and which genes are responsible for the high cognitive abilities is still largely unclear. The better our understanding of the role of genes in brain development, the more likely it will be that we will be able to develop treatments for serious brain diseases. 

Researchers are approaching these questions by knocking out or activating individual genes and thus drawing conclusions about their role in brain development. To avoid animal experiments as far as possible, brain organoids are used as an alternative. These three-dimensional cell structures, which are only a few millimeters in size, reflect different stages of brain development and can be genetically modified. However, such modifications are usually very complex, lengthy and costly. Researchers at the German Primate Center (DPZ) – Leibniz Institute for Primate Research in Göttingen have now succeeded in genetically manipulating brain organoids quickly and effectively.