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For the first time, scientists have begun to figure out why the disfiguring skin lesions caused by cutaneous leishmaniasis don’t hurt.

Researchers analyzed leishmaniasis lesions on mouse skin to detect metabolic signaling pathways that differed from uninfected mice. Results suggested the parasites that cause the disease change pain perception—presumably as a way to delay treatment and promote their own survival.

“No one knows why these lesions are painless—but it has been thought that the parasite somehow manipulates the host physiological system,” said Abhay Satoskar, senior author of the study and professor of pathology at The Ohio State University College of Medicine.

Introduction to spatial genomics The power of single-cell resolution Mapping the blueprint of health Case study: Bio-Techne Challenges and future prospects References Further reading

Spatial genomics is a cutting-edge field that combines genomics and spatial analysis to investigate the role of genomic features in disease at single-cell resolution.

Spatial genomics is a field of study that focuses on analyzing the spatial organization of genomic features within intact tissues. It involves the simultaneous analysis of various molecular components, including genomic DNA and RNA, through transcriptomic analysis and epigenetic modifications within their spatial context. These techniques aim to reveal the spatial relationships between the different genomic elements and provide insights into the organization and function of single cells within tissues, enabling the molecular connection of a particular genotype to its phenotype.

Researchers at the Francis Crick Institute, UCL and MSD have identified a potential treatment target for a genetic type of epilepsy.

Developmental and epileptic encephalopathies are rare types of epilepsy that start in early childhood. One of the most common types of genetic epilepsy, CDKL5 deficiency disorder (CDD), causes seizures and impaired development. Children are currently treated with generic antiepileptic drugs, as there aren’t yet any disease-targeting medications for this disorder.

CDD involves losing the function of a gene producing the CDKL5 enzyme, which phosphorylates proteins, meaning it adds an extra phosphate molecule to alter their function. Until now, researchers have not been sure how in CDKL5 cause CDD.

Researchers have succeeded in restoring lost brain function in mouse models of stroke using small molecules that in the future could potentially be developed into a stroke recovery therapy. “Communication between nerve cells in large parts of the brain changes after a stroke and we show that it can be partially restored with the treatment,” says Tadeusz Wieloch, senior professor of neurobiology at Lund University in Sweden.

“Concomitantly, the rodents regain lost somatosensory functions, something that around 60 per cent of all stroke patients experience today. The most remarkable result is that the treatment began several days after a stroke,” Wieloch continues.

In an ischemic stroke, lack of blood flow to the brain causes damage, which rapidly leads to nerve cell loss that affects large parts of the vast network of nerve cells in the brain.