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Category: bioengineering

Engineered protein markers read living brain gene activity in monkeys via blood

Gene therapy has been successfully used to treat a number of diseases, including immune deficiencies, hereditary blindness, hemophilia and, recently, Huntington’s disease, a fatal neurological disorder.

An advance reported in the journal Neuron adds to the technique’s growing track record of evidence supporting the view that it could unlock powerful, personalized therapies: Rice University bioengineer Jerzy Szablowski and collaborators in Vincent Costa’s lab at Emory University found that released markers of activity (RMAs) — engineered proteins designed to cross the blood-brain barrier and persist in the blood for hours at a time, providing a reliable and noninvasive way to get information about gene expression in the brain — work just as well in monkeys as they do in mice.

On the route from laboratory discovery to lifesaving treatment, large animal model studies are a critical part of the process. Most research never reaches this stage.

Bioengineered neuronal ‘circuit board’ mimics conditions of the human brain

A new bioengineered neuronal circuit board “BioConNet” allows scientists to artificially engineer human brain-like wiring at scale and can be used to engineer any possible circuit. The fully programmable, open-source system allows generation of large-scale circuits, while maintaining the ability to focus on single connections between neurons.

This is a key advance in engineering human-like neural circuits as it allows for a new level of wiring complexity compared to previous systems. BioConNet allows scientists increased control over wiring in the culture compared to existing methods such as organoids and commercially available systems. The research is published in the journal Advanced Healthcare Materials.

“By combining engineering and neurobiology with the most recent stem cell culture techniques, we can now create human-specific, functional, large-scale complex neural circuits in the lab,” said senior author, Dr. Andrea Serio, Reader in Neural Tissue Engineering, Group Leader at the UK Dementia Research Institute (UK DRI) at King’s and Senior Group Leader at the Crick.

Why do microbes team up? A new model explains nutrient sharing in fluctuating environments

Depending on others for something you need may feel like a risky proposition—and perhaps a human one. It is actually a survival strategy found in the microbial world, and far more frequently than one might expect. Discovering why is key to understanding how microbes form stable communities across medical, industrial, and ecological settings.

A new study by bioengineering professor Sergei Maslov (CAIM co-leader), computational scientist Ashish George, and biology professor Tong Wang explores why interdependence can be such a winning move for microbial communities. Their work, published in Cell Systems, demonstrated that a mathematical model of how bacteria produce and share resources accurately predicted the outcome of experiments with living E. coli strains.

The researchers’ collaboration began during their time as colleagues at the Carl R. Woese Institute for Genomic Biology at the University of Illinois Urbana-Champaign. George continued the collaboration in his position at the Broad Institute; Wang, in his appointment at Purdue University. Maslov, who led the study, remains at Illinois and is an affiliate member of the National Institute for Theory and Mathematics in Biology.

Genetic defect that weakens esophageal lining identified!

But the molecular factors responsible for the onset of Barrett’s esophagus remain poorly understood.

The findings, published in Nature Communications, combined family studies, laboratory experiments and genetically engineered mouse models to identify and understand how genetic defects contribute to disease development.

The team sequenced and analyzed genetic material of 684 people from 302 families where multiple members developed Barrett’s esophagus or esophageal cancer. They discovered that a subset of affected family members carry inherited mutations in a gene called VSIG10L.

“We found that this gene acts like a quality control system for the esophageal lining,” said the lead researcher. “When it’s defective, the cells do not mature properly and the protective barrier in the esophageal lining becomes weak, allowing stomach bile acid to cause tissue changes that enhances the risk of developing Barrett’s esophagus.”

When researchers genetically engineered mice with human-equivalent VSIG10L mutations, they found that the esophageal lining became disrupted structurally and molecularly, according to the author. The study found that when the mice were exposed to bile acid, they developed Barrett’s-like disease over time, effectively replicating the disease’s progression in humans.

These genetically engineered mice also represent the first animal model for Barrett’s esophagus based directly on human genetic predisposition to the disease, the author said.

With VSIG10L shown to be a key gene in maintaining esophageal health, family members can now be screened for genetic variants to identify those at a high-risk of developing Barrett’s esophagus or esophageal cancer. ScienceMission sciencenewshighlights.

Continue reading “Genetic defect that weakens esophageal lining identified!” | >

How chronic inflammation rewires macrophages

TIL therapy for glioblastoma.

Tumor infiltrating lymphocyte (TIL) therapy has demonstrated encouraging efficacy in melanoma and nonsmall-cell lung cancer (NSCLC), and is now being explored for glioblastoma despite its immunologically ‘cold’ microenvironment.

Recent studies confirm that functional TILs can be expanded from cold tumors such as glioblastoma, including solid tumor resections and aspirates, overcoming previous feasibility concerns.

Advances in cytokine support, gene editing, and artificial antigen-presenting cells (APCs) are improving TIL persistence, cytotoxicity, and manufacturing scalability.

Focused ultrasound and nanoparticle delivery offer innovative solutions to enhance TIL infiltration across the blood– brain barrier. Integration of spatial multi-omics enables high-resolution mapping of immune niches and identification of tumorreactive clones.

Combination strategies with checkpoint blockade, myeloid modulation, and oncolytic virotherapy are emerging as rational paths to enhance TIL efficacy sciencenewshighlights ScienceMission https://sciencemission.com/TIL-therapy-17895

Continue reading “How chronic inflammation rewires macrophages” | >

Post-Humans of All Tomorrows-3D Size Comparison

In All Tomorrows by C. M. Kosemen, also known as Nemo Ramjet, humanity’s distant descendants are reshaped across millions of years into wildly divergent “post-human” species after being genetically engineered by the godlike alien Qu. These forms range from tiny, almost vermin-like organisms and sessile, colony-bound beings to aquatic leviathans, aerial gliders, and towering, heavily built giants as each adapted to extreme planetary environments and radically different evolutionary pressures. Some retain echoes of recognizable humanity, while others are so transformed they blur the line between animal, ecosystem, and living architecture. In this size comparison, we’ll explore the full spectrum of these post-human forms, from the smallest engineered remnants to the most massive macro-organic descendants.

Credits:
https://all-tomorrows.fandom.com/wiki/Qu.
https://speculativeevolution.fandom.com/wiki/All_Tomorrows.

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Chitosan-nickel biomaterial becomes stronger when wet, and could replace plastics

A new study led by the Institute for Bioengineering of Catalonia (IBEC) has unveiled the first biomaterial that is not only waterproof but actually becomes stronger in contact with water. The material is produced by the incorporation of nickel into the structure of chitosan, a chitinous polymer obtained from discarded shrimp shells. The development of this new biomaterial marks a departure from the plastic-age mindset of making materials that must isolate from their environment to perform well. Instead, it shows how sustainable materials can connect and leverage their environment, using their surrounding water to achieve mechanical performance that surpasses common plastics.

Plastics have become an integral part of modern society thanks to their durability and resistance to water. However, precisely these properties turn them into persistent disruptors of ecological cycles. As a result, unrecovered plastic is accumulating across ecosystems and becoming an increasingly ubiquitous component of global food chains, raising growing concerns about potential impacts on human health.

In an effort to address this challenge, the use of biomaterials as substitutes for conventional plastics has long been explored. However, their widespread adoption has been limited by a fundamental drawback: Most biological materials weaken when exposed to water. Traditionally, this vulnerability has forced engineers to rely on chemical modifications or protective coatings, thereby undermining the sustainability benefits of biomaterial-based solutions.

Toward regenerative bioprinting: Magnetic mixer enables scalable manufacturing of 3D-printed tissues

3D bioprinting, in which living tissues are printed with cells mixed into soft hydrogels, or “bio-inks,” is widely used in the field of bioengineering for modeling or replacing the tissues in our bodies. The print quality and reproducibility of tissues, however, can face challenges. One of the most significant challenges is created simply by gravity—cells naturally sink to the bottom of the bioink-extruding printer syringe because the cells are heavier than the hydrogel around them.

“This cell settling, which becomes worse during the long print sessions required to print large tissues, leads to clogged nozzles, uneven cell distribution, and inconsistencies between printed tissues,” explains Ritu Raman, the Eugene Bell Career Development Professor of Tissue Engineering and assistant professor of mechanical engineering at MIT.

“Existing solutions, such as manually stirring bioinks before loading them into the printer, or using passive mixers, cannot maintain uniformity once printing begins.”

How a key receptor tells apart two nearly identical drug molecules

G-protein-coupled receptors (GPCRs) are one of the largest families of cell surface proteins in the human body that recognize hormones, neurotransmitters, and drugs. These receptors regulate a wide range of physiological processes and are the targets of more than 30% of currently marketed drugs. The histamine H1 receptor (H1R) is one such GPCR subtype that plays a key role in mediating allergic reactions, inflammation, vascular permeability, airway constriction, wakefulness, and cognitive functions in the human body. While antihistamines primarily target H1R, current drugs can exhibit limited therapeutic efficacy, prompting researchers to look at H1R ligands from new perspectives.

Recently, the importance of drug design based not only on the affinity or binding energy between a compound and its target protein, but also on its components, enthalpy, and entropy, has been recognized as crucial for rational drug design. In particular, enthalpy–entropy compensation has emerged as a key concept for understanding ligand selectivity and isomer specificity. However, direct experimental measurement of these thermodynamic parameters has been limited to cell surface proteins, such as GPCRs.

Addressing this gap, a research team led by Professor Mitsunori Shiroishi from the Department of Life System Engineering, Tokyo University of Science (TUS), Japan, systematically investigated the binding thermodynamics of the H1R. The team included Mr. Hiroto Kaneko (first-year doctoral student) and Associate Professor Tadashi Ando from TUS, among others. Their study was published online in ACS Medicinal Chemistry Letters on January 26, 2026.

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