Hemin-Induced Transient Senescence Via DNA Damage Response: A Neuroprotective Mechanism Against Ferroptosis in Intracerebral Hemorrhage.

Intracerebral hemorrhage (ICH) poses acute fatality and long-term neurological risks due to hemin and iron accumulation from hemoglobin breakdown. Our observation that hemin induces DNA double-strand breaks (DSBs), prompting a senescence-like phenotype in neurons, necessitating deeper exploration of cellular responses. Using experimental ICH models and human ICH patient tissue, we elucidate hemin-mediated DNA damage response (DDR) inducing transient senescence and delayed expression of heme oxygenase (HO-1).

Deficiency of m A RNA methylation promotes ZBP1-mediated cell death.

m A RNA methylation suppresses the immunostimulatory potential of endogenous RNA. Deficiency of m A provokes inflammatory responses and cell death, but the underlying mechanisms remain elusive. Here we showed that the noncoding RNA 7SK gains immunostimulatory potential upon m A depletion and subsequently activates the RIG-I/MAVS axis to spark interferon (IFN) signaling cascades.

Extraction of Radiological Characteristics From Free-Text Imaging Reports Using Natural Language Processing Among Patients With Ischemic and Hemorrhagic Stroke: Algorithm Development and Validation.

Background: Neuroimaging is the gold-standard diagnostic modality for all patients suspected of stroke. However, the unstructured nature of imaging reports remains a major challenge to extracting useful information from electronic health records systems. Despite the increasing adoption of natural language processing (NLP) for radiology reports, information extraction for many stroke imaging features has not been systematically evaluated.

Minimally Invasive Approaches in Reoperations after Conventional Craniotomies : Case Series.

Objective: Reoperations are part of neurosurgical practice. In these cases, an already formed craniotomy seems the most logical and appropriate. However, reoperations via large approaches can be quite traumatic for the patient.

RNA/DNA Binding Protein TDP43 Regulates DNA Mismatch Repair Genes with Implications for Genome Stability.

TAR DNA-binding protein 43 (TDP43) is increasingly recognized for its involvement in neurodegenerative diseases, particularly amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). TDP43 proteinopathy, characterized by dysregulated nuclear export and cytoplasmic aggregation, is present in most ALS/FTD cases and is associated with a loss of nuclear function and genomic instability in neurons. Building on prior evidence linking TDP43 pathology to DNA double-strand breaks (DSBs), this study identifies a novel regulatory role for TDP43 in the DNA mismatch repair (MMR) pathway.