This resource is a video abstract of a research paper created by …
This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:
"The ability to label and manipulate proteins in the body is essential to modern biological research. Unfortunately, current methods, such as tagging with antibodies, are often inefficient and expensive. Even worse, researchers are realizing that many of the antibodies available just simply don’t work. Now, a new molecular tool could help researchers break through that barrier. Researchers in the Soderling Laboratory of the Cell Biology Department at Duke University, have developed a high-throughput system capable of modifying entire panels of proteins using a new dual-vector gene-editing approach. Dubbed Homology-independent Universal Genome Engineering, this system allows for the dynamic visualization and functional manipulation of proteins both in vitro and in vivo, including in neurons. This is HiUGE. HiUGE isn’t the first protein-modifying system to rely on gene editing..."
The rest of the transcript, along with a link to the research itself, is available on the resource itself.
This resource is a video abstract of a research paper created by …
This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:
"One hallmark of neurodegenerative diseases such as Alzheimer's and Parkinson's is protein accumulation in the brain. That accumulation is driven by structural modification of the cellular prion protein. which produces self-generating particles in the brain. Neuronal cell death caused by these protein clusters occurs through autophagy, the body’s way of degrading damaged cells. Unfortunately, the pathways mediating prion-driven autophagy in neurons remain unclear. A recent study evaluated the role of calcium signaling – a common signaling pathway affected by prion proteins. Using neuronal cells from mice, researchers measured calcium signaling and the levels of proteins involved in metabolic stress and autophagy. Their results showed that human prion peptide increased the concentration of calcium in neurons. Inhibiting this prion-mediated calcium uptake in neurons prevented autophagic cell death. and preserved the activity of a protein called AMPK, which is involved in maintaining energy balance in cells..."
The rest of the transcript, along with a link to the research itself, is available on the resource itself.
Building on their understanding of graphs, students are introduced to random processes …
Building on their understanding of graphs, students are introduced to random processes on networks. They walk through an illustrative example to see how a random process can be used to represent the spread of an infectious disease, such as the flu, on a social network of students. This demonstrates how scientists and engineers use mathematics to model and simulate random processes on complex networks. Topics covered include random processes and modeling disease spread, specifically the SIR (susceptible, infectious, resistant) model.
This resource is a video abstract of a research paper created by …
This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:
"For nearly 25 years, scientists have known of the neuroprotective properties associated with the protein called prosaposin. But exactly how prosaposin exerts these effects has been a matter of debate. Initial research using a neuroactive fragment of the protein, called TX14(A), identified two closely related receptors thought to mediate the actions of prosaposin. But this work was later challenged. Now, an international team of scientists has reported strong evidence that prosaposin does activate these receptors, which may help pave the way for a new class of neuroprotective drugs. Uncertainty over the status of prosaposin as an endogenous ligand for GPR37L1 and GPR37 has stemmed from the use of widely varying experimental conditions. The main inconsistency with past work was the use of cell lines derived from ovary, kidney or yeast to study the receptors. But this creates a physiological mismatch, as the receptors are almost exclusively expressed in the brain..."
The rest of the transcript, along with a link to the research itself, is available on the resource itself.
This resource is a video abstract of a research paper created by …
This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:
"Quantum materials are opening up a realm of possibilities in materials research. Among the best known examples are superconductivity and quantum computing. But that’s only the beginning. The same properties that make these materials unique are also enabling researchers to demystify the inner workings of the human brain. So what makes quantum materials well suited for this purpose? Unlike the free-flowing electrons in ordinary conductors or semiconductors, electrons in quantum materials show correlated behavior. That in itself has been the focus of intense physics research. But the upshot for brain research is tunable electronic behavior that can mimic the electronic signaling of neurons and the synapses between them. Most importantly, quantum materials can simulate synaptic plasticity. Plasticity is the biological ability that makes learning and memory formation possible. It’s all about timing. Connections between neurons that fire within a short, milliseconds-long time window grow stronger..."
The rest of the transcript, along with a link to the research itself, is available on the resource itself.
This series of research talks by members of the Department of Brain …
This series of research talks by members of the Department of Brain and Cognitive Sciences introduces students to different approaches to the study of the brain and mind. Topics include:
From Neurons to Neural Networks Prefrontal Cortex and the Neural Basis of Cognitive Control Hippocampal Memory Formation and the Role of Sleep The Formation of Internal Modes for Learning Motor Skills Look and See: How the Brain Selects Objects and Directs the Eyes How the Brain Wires Itself
Why do teenagers act the way they do? This video segment from …
Why do teenagers act the way they do? This video segment from FRONTLINE: Inside the Teenage Brain explores the work scientists are doing to explain some of the mysteries of teenage behavior.
Students learn how neurons send and receive messages, and then build a …
Students learn how neurons send and receive messages, and then build a model neuron. This activity is from the Brain Chemistry Teacher's Guide. Lessons in the guide are most appropriate for students in grades 5-10.
This resource is a video abstract of a research paper created by …
This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:
"Wnt signaling plays key roles in many processes, including cell polarity, proliferation, differentiation, and migration. The pathway is centrally involved in neurite and synapse development and maintenance. Wnt activity can be inhibited by Porcupine, an acylase that modifies Wnt ligands. A new study sought to understand how Wnt ligands affect neurite development. Using Wnt-C59, a Porcupine inhibitor, researchers blocked the secretion of endogenous Wnts in rat embryonic hippocampal neurons. They found that inhibiting Porcupine changed the morphology of the dendritic arbors and neurites of hippocampal neurons, while axonal polarity was not affected. β-catenin and Wnt3 levels decreased with Porcupine inhibition, while GSK-3β increased. Adding exogenous Wnt3a, 5a, and 7a ligands rescued the changes in neuronal morphology. Wnt3a restored neurite length to near the control, while Wnt7a increased the neurite length beyond that of the control..."
The rest of the transcript, along with a link to the research itself, is available on the resource itself.
This resource is a video abstract of a research paper created by …
This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:
"In nerve cells, the waxy molecule ceramide plays roles in both cellular differentiation and death, but a new study shows those roles could vary based on how ceramide is formed. Ceramide is generated via 3 pathways: newly from palmitoyl-CoA and serine, from the breakdown of sphingomyelin, and through the endosomal salvage pathway. Experiments showed that blocking ceramide synthesis did not alter ceramide levels in PC12 cells, which require nerve growth factor (NGF) to survive and differentiate, but blocking synthesis did decrease ceramide levels in TrkA cells, which differentiate spontaneously. Blocking sphingomyelin breakdown, however, inhibited differentiation and reduced ceramide in both cell lines. Without NGF, PC12 cells begin to atrophy and die, and preventing sphingomyelin breakdown did not protect them, but it did suppress rising ceramide levels to some degree versus controls..."
The rest of the transcript, along with a link to the research itself, is available on the resource itself.
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