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Common nanostructures may explain shared photoproperties in two widespread dark materials

A newly developed framework for understanding the photoproperties of both natural organic matter and eumelanin, a natural pigment responsible for dark colors in organisms, may inspire advanced sustainable technologies, scientists say.

Although they are some of the most widespread substances on Earth, not much is known about eumelanin or natural organic matter (NOM)—a dark-colored substance formed by the decomposition of biological material. In humans, eumelanin is a vital pigment in skin and other tissues that protects cells from damage caused by ultraviolet radiation. In nature, NOM gives rivers and soils their color and affects light-driven reactions like photosynthesis.

Although these compounds have been studied individually for decades, researchers in a new study, by scrutinizing them alongside each other, have shown that eumelanin and NOM have common properties beyond their dark colors.

Brainwide blood volume reflects opposing neural populations

An interesting new approach to more accurately predicting blood flow in the mouse brain based on the activity of neurons correlated positively or negatively with arousal (as measured by whisking). Neuropixels and functional ultrasound imaging were used to simultaneously record from neurons and map blood flow, allowing the authors to derive their model.

Combined functional ultrasound imaging and Neuropixels recording of mouse brains identify two neuronal populations with opposing arousal-related activity and distinct haemodynamic response functions, that occur throughout the brain.

Resilience to autosomal dominant Alzheimer’s disease in a Reelin-COLBOS heterozygous man

Fascinating case study on the neuroprotective effects of a mutant reelin allele (RELN–COLBOS) which delayed disease progression in a patient with autosomal dominant Alzheimer’s disease (ADAD). A promising therapeutic target!

Case report of an individual heterozygous for a rare RELN–COLBOS variant that confers resilience, via a gain-of-function mechanism, to Alzheimer’s disease.

Newfound biomarkers may someday help clinicians better detect—and possibly cure—Lyme disease

Lyme disease can be easiest to treat in its earliest stages, but current tests often miss infections during that critical window and cannot tell whether bacteria are still present or were cleared years ago. New research led by Tufts University School of Medicine suggests that a group of immune molecules called anti-lipid antibodies may address these shortcomings.

The findings, published in Infection and Immunity, could lead to improved tests that identify Lyme disease earlier, when antibiotics can best prevent more debilitating disease. They also may help clinicians better identify patients who continue to experience symptoms of infection after treatment—and potentially find new drug targets to help them.

Nearly half a million Americans are diagnosed and treated for Lyme disease each year. Caused by the bacterium Borrelia burgdorferi and spread through the bite of infected blacklegged ticks (also known as deer ticks), the disease can lead to arthritis, neurological problems and heart complications if untreated.

Common brain cancer mutation changes DNA shape to drive progression, exposing therapeutic target

A new study from researchers at The University of Texas MD Anderson Cancer Center has uncovered how one of the most common genetic alterations in glioma rewires the cancer cell genome to fuel tumor progression, suggesting a potential new therapeutic strategy for patients with ATRX-mutant gliomas.

The findings show that mutations in the ATRX gene fundamentally reprogram the epigenome and change the three-dimensional structure of chromatin, creating new interactions that activate developmental programs that tumors exploit to grow and spread. Targeting one of the genes downstream of ATRX in preclinical models—particularly in the HOXA family—slowed cancer progression.

The study, published in Nucleic Acids Research, was co-led by Jason Huse, M.D., Ph.D., professor of Anatomic Pathology, and Kunal Rai, Ph.D., professor of Genomic Medicine, with major contributions from Prit Benny Malgulwar, Ph.D., instructor of Translational Molecular Pathology, Anand Singh, Ph.D., senior research scientist in Genomic Medicine, and Ajay Saw, Ph.D., previous postdoctoral fellow in Genomic Medicine.

Photoswitch drug shows early signs of restoring light sensitivity in severely damaged retinas in first human trial

Adelaide University researchers have carried out the first in-human trial of a new type of treatment for a leading cause of blindness in working age adults, with promising results.

Retinitis pigmentosa is a genetic condition in which the retinal cells responsible for detecting light don’t work properly, resulting in progressive blindness. Current treatment options for later stages of the disease are limited, and there’s no cure. Now, a new approach to treating the disease is providing fresh hope. Working with researchers from the University of Washington, University of Adelaide experts carried out a small pilot trial to see whether a potential therapy based on a molecule could be safely tolerated by humans.

They found that when the small molecule was injected into the eye, it revived some of the damaged retinal cells, making them sensitive to light again. This happened even after the normal light-sensing cells had been lost.

New tumor map identifies high-risk B-cell lymphoma standard therapy may miss

Researchers led by Universitätsmedizin Frankfurt and Goethe University Frankfurt have identified how particularly aggressive forms of lymphoma can be recognized. By combining genetic and proteomic analyses, the scientists identified biological characteristics of tumors, particularly in high-risk patients for whom standard therapy offers little chance of cure. In the future, such patients could receive alternative, more effective therapies directly. In addition, experimental laboratory research provided initial clues to potential therapeutic targets. The study is published in Cancer Cell.

With more than 150,000 new cases worldwide each year, diffuse large B-cell lymphoma (DLBCL) is the most common aggressive form of lymphoma. Following diagnosis, patients typically receive a standard treatment regimen consisting of a therapeutic antibody and chemotherapy (R-CHOP or Pola-R-CHP), and nearly two-thirds of patients have a good chance of being cured. However, more than one-third of patients experience a relapse after treatment, or their tumors fail to respond to therapy, requiring alternative treatments such as CAR T-cell therapy.

The varying effectiveness of standard therapy is due to the considerable molecular heterogeneity of the disease. Researchers have therefore long been searching for molecular tumor characteristics that would allow them to distinguish among different DLBCL subtypes and treat them more specifically.

Forcing cancer cells to die can alert the immune system to enhance anti-tumor attack

Unlike accidental cell death, some cells can actively decide to die through a controlled process. This is called programmed cell death and can occur in different forms, including apoptosis and necroptosis. Cells use this process when they are damaged, stressed, becoming cancerous, or infected by harmful microbes. This self-destruction mechanism helps to protect the body, but it is also involved in many diseases, such as infections, inflammatory conditions and cancer.

A major problem in cancer is that some tumors and cancer cells learn how to avoid apoptosis, allowing them to survive when they should die. This resistance can make cancer treatments less effective, especially in advanced or spreading (metastatic) cancers.

A research team led by Prof. Dr. Sjoerd van Wijk, Professor for Cell Biology at the Institute for Physiology and Cell Biology of the University of Veterinary Medicine (TiHo), and Dr. Francesco Pampaloni of the Goethe University Frankfurt, have studied a type of programmed cell death called necroptosis in advanced breast cancer. The scientists used patient-derived organoids, which are tiny 3D mini-tumors grown in the lab from real patients’ cancer cells. These mini tumors closely resemble the original cancer, making them useful for testing treatments and cell biology experiments.

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