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New research clears the way to healing lung diseases

Pulmonary fibrosis is a deadly disease in which scar tissue grows in the lungs, making breathing more difficult. Approximately 2,170 Australians are diagnosed annually with idiopathic pulmonary fibrosis (IPF), a form of the disease with no known cause and very few treatments.

“In pulmonary fibrosis, the normal wound-healing process in the body goes wrong. Instead of repairing damaged tissue, it starts to produce scar tissue in the lungs,” said Associate Professor Gang Liu from the University of Technology Sydney (UTS) School of Life Sciences.

“People with idiopathic pulmonary fibrosis have a very short survival time, usually only two to five years from diagnosis. Only two drugs are approved to treat it, and neither can reverse the scarring and cure the disease.”

Feasibility evaluation of tumor treating fields for brainstem gliomas

Tumor treating fields (TTFields) are FDA-approved for supratentorial glioblastoma, but feasibility in infratentorial tumors remains poorly defined. This simulation study evaluated TTFields dose in brainstem gliomas using patient-specific modeling with scalp-only transducer arrays.

MRI and CT imaging from seven patients with brainstem gliomas were used for TTFields planning with MAXPOINT® (Novocure, Switzerland). Clinical target volume (CTV) was defined as enhancing tumor on T1 post-contrast MRI (Gross tumor volume, GTV) plus a 3 mm peritumoral expansion. The platform optimized scalp-only array layouts, and finite element calculations generated maps of local minimum field intensity (LMiFI, V/cm) and local minimum power density (LMiPD, mW/cm³). Values were compared against a standard, unplanned layout using one-sided paired t-tests, with LMiFI ≥ 1.0 V/cm as a therapeutic reference.

MAXPOINT-optimized layouts achieved significantly higher LMiFI than the standard layout across all regions (all p ≤ 0.019). GTV median LMiFI was 1.1 vs. 1.0 V/cm (p = 0.019). CTV median LMiFI was 1.1 vs. 1.0 V/cm (p = 0.002). Brainstem median LMiFI was 1.3 vs. 1.1 V/cm (p = 0.002). Posterior fossa showed the largest difference: median LMiFI 1.5 vs. 1.2 V/cm (p 0.001). All optimized LMiFI values met or exceeded the therapeutic reference. LMiPD was also significantly higher with MAXPOINT® across all regions (all p ≤ 0.006).

Finding the RNA aptamer in the haystack that could improve treatment for Parkinson’s

Synucleinopathies are a group of neurodegenerative disorders that include serious conditions such as Parkinson’s disease and dementia with Lewy bodies. There are currently no cures for these disorders, and treatment is limited to mitigating symptoms. Recently, antibody-based therapies have attracted considerable attention, but alternative approaches are still necessary.

Therapy development for synucleinopathies tends to target the alpha-synuclein protein, αSyn, the abnormal aggregation of which is a hallmark of these diseases. However, targeting this protein using conventional drug discovery strategies is stymied by the molecule’s lack of a stable three-dimensional structure, which promotes aggregation.

Interested in understanding how abnormal protein aggregation drives neurodegeneration, a team of researchers at Kyoto University had an idea that was both scientifically intriguing and therapeutically promising: Could RNA aptamers—often described as “chemical antibodies”—directly recognize αSyn’s disordered regions and suppress pathological aggregation?

Decoding of amidated aromatic Cterminus and sulfation by cholecystokinin receptors reveals conserved and divergent evolutionary mechanisms

Understanding how evolutionarily related receptors preserve recognition principles for conserved peptide post-translational modifications (PTMs) while acquiring new selectivity remains central to neuropeptide-G protein-coupled receptor (GPCR) biology. The Aplysia cholecystokinin (CCK) system provides an informative model, as its peptides combine two representative PTM-related features: an amidated aromatic C-terminus (RFamide/DFamide), and a dual-tyrosine sulfation pattern exceeding the single-site architecture typical of vertebrates.

Gene therapy restores key fragile X traits in preclinical study

A gene therapy designed to replace the missing protein that causes fragile X syndrome restored several disease-relevant traits in a mouse model, according to a new study published in Gene Therapy.

Fragile X syndrome is the most common inherited form of intellectual disability and a leading single-gene condition associated with autism. There is no cure, and current care focuses on managing symptoms such as anxiety, sensory sensitivity, hyperactivity, developmental seizures and learning challenges.

The study, led by investigators at Cincinnati Children’s and collaborators at Forge Biologics, tested adeno-associated viral vectors carrying human FMR1, the gene silenced in fragile X syndrome. After testing several candidates, the team found an approach that produced the FMRP protein in key brain regions and improved multiple phenotypes in Fmr1 knockout mice.

3Dprinted bridge points the way to greener construction

Concrete is the most widely used building material on Earth, and producing it is one of the largest single sources of carbon emissions. One promising way to reduce its environmental footprint is to 3D-print concrete, laying it down bead by bead like a giant icing-piping robot. This process eliminates the labor-intensive formwork of pouring it into molds, and places the material only where a structure needs it.

But many of the most efficient designs created by computers are impossible for today’s printers to build. Engineers use a technique called topology optimization to find the strongest structure that uses the least amount of material. But those mathematically ideal designs, with their intricate, spider-web shapes, don’t account for the physical limitations of large-scale concrete printers with their thick nozzles, limited turning, and need to print in one continuous motion.

Now a team of MIT researchers has developed a way to close that gap. Their framework, described in a new article in Additive Manufacturing, bakes a printer’s real fabrication limits directly into the optimization, so the design that comes out is one a machine can build and print with little or no manual redesign. They demonstrated it by designing, printing, and load-testing a 2.3-meter concrete bridge and found that today’s printing hardware, not the concrete itself, limits how light a structure can be.

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