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Despite its success, FNP has some limitations: it can’t create stable particles larger than 400 nm, the maximum drug content is about 70 percent, the output is low, and it can only work with very hydrophobic (water-repelling) molecules. These issues arise because the particle core formation and particle stabilization happen simultaneously in FNP. The new SNaP process overcomes these limitations by separating the core formation and stabilization steps.

In the SNaP process, there are two mixing steps. First, the core components are mixed with water to start forming the particle core. Then, a stabilizing agent is added to stop the core growth and stabilize the particles. This second step must happen quickly, less than a few milliseconds after the first step, to control the particle size and prevent aggregation. Current SNaP setups connect two specialized mixers in series, controlling the delay time between steps. However, these setups face challenges, including high costs and difficulties in achieving short delay times needed for small particle formation.

A new approach using 3D printing has solved many of these challenges. Advances in 3D printing technology now allow the creation of precise, narrow channels needed for these mixers. The new design eliminates the need for external tubing between steps, allowing for shorter delay times and preventing leaks. The innovative stacked mixer design combines two mixers into a single setup, making the process more efficient and user-friendly.

Can you pass me the whatchamacallit? It’s right over there next to the thingamajig.

Many of us will experience “lethologica”, or difficulty finding words, in everyday life. And it usually becomes more prominent with age.

Frequent difficulty finding the right word can signal changes in the brain consistent with the early (“preclinical”) stages of Alzheimer’s disease – before more obvious symptoms emerge.

Scientists at the Okinawa Institute of Science and Technology (OIST), the National Institute of Information and Communications Technology, and the University of Tokyo have found a mathematical connection between spatial navigation and language processing, creating a model called “Disentangled Successor Information” (DSI).

This model generates patterns that closely resemble the activity of actual brain cells involved in both spatial awareness (place cells and grid cells) and concept recognition (concept cells).

The DSI model shows that the hippocampus and entorhinal cortex— previously known primarily for —likely use comparable computational processes to handle both physical spaces and meaningful ideas or words. Using this shared framework, both types of information can be processed through similar mathematical computations, which could be achieved in the brain by partial activation of specific groups of neurons.

Mind Control: Past and Future https://www.hks.harvard.edu/sites/default/files/2025-01/24_Meier_02.pdf


On Jan. 28, 2024, Noland Arbaugh became the first person to receive a brain chip implant from Neuralink, the neurotechnology company owned by Elon Musk. The implant seemed to work: Arbaugh, who is paralyzed, learned to control a computer mouse with his mind and even to play online chess.

The device is part of a class of therapeutics, (BCIs), that show promise for helping people with disabilities control prosthetic limbs, operate a computer, or translate their thoughts directly into speech. Current use of the technology is limited, but with millions of global cases of spinal cord injuries, strokes, and other conditions, some estimates put the market for BCIs at around $400 billion in the U.S. alone.

A new discussion paper from the Carr Center for Human Rights welcomes the potential benefits but offers a note of caution drawn from the past, detailing unsettling parallels between an era of new therapies and one of America’s darkest chapters: experiments into psychological manipulation and mind control.

For decades, scientists have focused on amyloid plaques—abnormal clumps of misfolded proteins that accumulate between neurons—as a therapeutic target for Alzheimer’s disease. But anti-amyloid therapies haven’t made strong headway in treating the devastating condition.

Now, researchers at Yale School of Medicine (YSM) are zeroing in on a byproduct of these plaques, called axonal spheroids, and exploring how to reverse their growth. They published their findings March 10 in Nature Aging.

Axonal spheroids are bubble-like structures on axons—the part of the neuron that sends messages through electrical impulses—that form due to swelling induced by amyloid plaques. Previous research at YSM has shown that as these spheroids grow, they block electricity conduction in the axons, which can hinder the ability to communicate with other neurons.

Summary: New research highlights a critical link between antibodies produced against Epstein-Barr virus (EBV) and the development of multiple sclerosis (MS). Scientists discovered that these viral antibodies mistakenly target a protein called GlialCAM in the brain, triggering autoimmune responses associated with MS.

The study also revealed how combinations of genetic risk factors and elevated viral antibodies further increase the risk of developing MS. These insights may pave the way for improved diagnostics and targeted therapies, enhancing our understanding of the genetic and immunological interplay underlying this debilitating disease.

Is an in-depth investigation featuring world renowned philosophers and scientists into the most profound philosophical debate of all time: Do we have free will?

Featuring: Sean Carroll, Daniel Dennett, Jerry Coyne, Dan Barker, Heather Berlin, Gregg Caruso, Massimo Pigliucci, Alex O’Conner, Coleman Hughes, Edwin Locke, Robert Kane, Rick Messing, Derk Pereboom, Richard Carrier, Trick Slattery, Dustin Kreuger, Steven Sharper, Donia Abouelatta.

Chapters.

Intro: — 0:00
Chapter 1: What is Free Will? — 4:19
Chapter 2: The Problem of Free Will — 15:29
Interlude: 22:33
Chapter 3: Libertarian Free Will — 23:16
Chapter 4: Compatibilism — 34:47
Chapter 5: Free Will Skepticism — 45:13
Interlude: The 3 Positions of Free Will — 55:45
Chapter 6: The Great Debate — 57:28
Chapter 7: Neuroscience — 1:07:28
Chapter 7: The Interaction Problem — 1:18:37
Chapter 8: Physics — 1:20:10
Chapter 8: Reduction & Emergence — 1:22:14
Chapter 9: Can We Have Determinism and Free Will? — 1:28:57
Chapter 10: Free Will and the Law — 1:45:57
Chapter 11: Should We Stop Using the Term Free Will? — 1:56:37
Outro: 2:00:38

Although it’s not the first time this was hypothesized, this study is the first time researchers looked at the presence of gingipains within the brains of diseased patients. Even more, the patients themselves were never even diagnosed with Alzheimer’s.

“Our identification of gingipain antigens in the brains of individuals with AD and also with AD pathology but no diagnosis of dementia argues that brain infection with P. gingivalis is not a result of poor dental care following the onset of dementia or a consequence of late-stage disease, but is an early event that can explain the pathology found in middle-aged individuals before cognitive decline,” the authors explained.

While this isn’t a one-size-fits-all answer to what causes Alzheimer’s, it’s a step in the right direction to finding the reasoning behind this life-altering disease.