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Many of us have been wracking our brains why Nvidia would spend a fortune – a whopping $40 billion – to acquire Arm Holdings, a chip architecture licensing company that generates on the order of $2 billion in sales – since the deal was rumored back in July 2020. As we sat and listened to the Arm Vision Day rollout of the Arm V9 architecture, which will define processors ranging from tiny embedded controllers in IoT device all the way up to massive CPUs in the datacenter, we may have figured it out.

There are all kinds of positives, as we pointed out in our original analysis ahead of the deal, in our analysis the day the deal was announced in September 2020, and in a one-on-one conversation with Nvidia co-founder and chief executive officer Jensen Huang in October 2020.

We have said for a long time that we believe that Nvidia needs to control its own CPU future, and even joked with Huang that it didn’t need to have to buy all of Arm Holdings to make the best Arm server CPU, to which he responded that this was truly a once-in-a-lifetime opportunity to create value and push all of Nvidia’s technologies – its own GPUs for compute and graphics and Mellanox network interface chips, DPU processors, and switch ASICs – through an Arm licensing channel to make them all as malleable and yet standardized as the Arm licensing model not only allows, but encourages.

Summary: All-trans retinoic acid, a vitamin A derivative, induces synaptic plasticity in human cortical neurons.

Source: eLife.

The brain has an enormous capacity to adapt to its environment. This ability to continuously learn and form new memories thanks to its malleability, is known as brain plasticity.

“Because contrast suppression is orientation-specific and relies on cortical processing, our results suggest that people experiencing a major depressive episode have normal retinal processing but altered cortical contrast normalization,” write the researchers in their paper.


We know that depression is linked to variations in the way our brains are wired, but new research suggests that people who are going through a depressive episode actually see the world around them differently.

And the team behind the study hopes that a better understanding of how visual information is processed in the brains of people with depression could help to inform our treatment approaches in the future.

The researchers wanted to analyze how the cerebral cortex – responsible for receiving messages from the five senses – handled an optical illusion, testing it out with 111 people who were experiencing major depressive episodes and 29 people who weren’t.

Sargramostim/GM-CSF is prescribed to boost white blood cells after cancer treatments or exposure to radiation. The protein stimulates the bone marrow to make more macrophages and granulocytes, specific types of white blood cells, and progenitor cells that repair blood vessels. These white blood cells circulate throughout the body and remove cells, bacteria and amyloid deposits and also repairing blood vessels.


The team carried out a randomized, double-blind, placebo-controlled Phase II trial (NCT01409915) to test the safety and efficacy of Sargramostim treatment in participants with mild-moderate Alzheimer’s disease.

Study participants were either administered Sargramostim at the standard FDA dose of 250 μg/m2/day by subcutaneous injection, or saline for five days a week for three weeks. The study included 20 participants in the test and placebo group. Most participants in the study were recruited and treated at CU Anschutz with a few from the University of South Florida. The CU Anschutz researchers then conducted and studied multiple neurological, neuropsychological, cell, cytokine, Alzheimer’s pathology biomarkers and neuroimaging assessments.

The investigators found that short-term Sargramostim treatment increased innate and other immune cells, modulated cytokine measures, and was safe and well-tolerated by participants. They also found cognition memory improved by almost two points in the 30 point Mini-Mental State Exam. Brain amyloid, tangles, neurodegeneration, and measures of blood biomarkers of Alzheimer’s disease, all improved toward normal.

More than 25 years ago, biologists in Arkansas began to report dozens of bald eagles paralyzed, convulsing, or dead. Their brains were pocked with lesions never seen before in eagles. The disease was soon found in other birds across the southeastern United States. Eventually, researchers linked the deaths to a new species of cyanobacteria growing on an invasive aquatic weed that is spreading across the country. The problem persists, with the disease detected regularly in a few birds, yet the culprit’s chemical weapon has remained unknown.

Today in Science, a team identifies a novel neurotoxin produced by the cyanobacteria and shows that it harms not just birds, but fish and invertebrates, too. “This research is a very, very impressive piece of scientific detective work,” says microbiologist Susanna Wood of the Cawthron Institute. An unusual feature of the toxic molecule is the presence of bromine, which is scarce in lakes and rarely found in cyanobacteria. One possible explanation: the cyanobacteria produce the toxin from a bromide-containing herbicide that lake managers use to control the weed.

The discovery highlights the threat of toxic cyanobacteria that grow in sediment and on plants, Wood says, where routine water quality monitoring might miss them. The finding also equips researchers to survey lakes, wildlife, and other cyanobacteria for the new toxin. “It will be very useful,” says Judy Westrick, a chemist who studies cyanobacterial toxins at Wayne State University and was not involved in the new research. “I started jumping because I got so excited.”

Summary: People with cerebral small vessel damage who also had a leaky blood-brain barrier had more tissue damage after two years than those whose blood-brain barrier was intact.

Source: AAN

As people age, changes in the tiniest blood vessels in the brain, a condition called cerebral small vessel disease, can lead to thinking and memory problems and stroke. These changes can also affect the blood-brain barrier, a layer of cells that protect the brain from toxins circulating in the blood.

Using an ordinary light microscope, MIT engineers have devised a technique for imaging biological samples with accuracy at the scale of 10 nanometers — which should enable them to image viruses and potentially even single biomolecules, the researchers say.

The new technique builds on expansion microscopy, an approach that involves embedding biological samples in a hydrogel and then expanding them before imaging them with a microscope. For the latest version of the technique, the researchers developed a new type of hydrogel that maintains a more uniform configuration, allowing for greater accuracy in imaging tiny structures.

This degree of accuracy could open the door to studying the basic molecular interactions that make life possible, says Edward Boyden, the Y. Eva Tan Professor in Neurotechnology, a professor of biological engineering and brain and cognitive sciences at MIT, and a member of MIT’s McGovern Institute for Brain Research and Koch Institute for Integrative Cancer Research.

Summary: Mimicking a muscular stress system can provide neuroprotection against aging in both the brain and retina. The signal helps prevent the buildup of misfolded protein aggregates.

Source: St. Jude Children’s Research Hospital.

How do different parts of the body communicate? Scientists at St. Jude are studying how signals sent from skeletal muscle affect the brain.

Stanford University neurobiologist Sergiu Pașca has been making brain organoids for about 10 years, and his team has learned that some of these tissue blobs can thrive in a dish for years. In the new study, they teamed up with neurogeneticist Daniel Geschwind and colleagues at the University of California, Los Angeles (UCLA), to analyze how the blobs changed over their life spans…

…They noticed that when an organoid reached 250 to 300 days old—roughly 9 months—its gene expression shifted to more closely resemble that of cells from human brains soon after birth. The cells’ patterns of methylation—chemical tags that can affix to DNA and influence gene activity—also corresponded to increasingly mature human brain cells as the organoids aged, the team reports today in Nature Neuroscience.


Organoids develop genetic signatures of postnatal brains, possibly broadening their use as disease models.