Acute brain injuries such as traumatic brain injury and stroke affect 85 million people a year worldwide, and many survivors suffer from long-term physical, cognitive, or psychosocial impairments. There are few FDA-approved therapies that are effective at preventing, halting, or ameliorating the state of disease in the brain after acute brain injury. To address this unmet need, one potential strategy is to leverage the unique physical and biological properties of nanomaterials. Decades of cancer nanomedicine research can serve as a blueprint for innovation in brain injury nanomedicines, both to emulate the successes and also to avoid potential pitfalls. In this review, we discuss how shared disease physiology between cancer and acute brain injuries can inform the design of novel nanomedicines for acute brain injuries. These disease hallmarks include dysregulated vasculature, an altered microenvironment, and changes in the immune system. We discuss several nanomaterial strategies that can be engineered to exploit these disease hallmarks, for example, passive accumulation, active targeting of disease-associated signals, bioresponsive designs that are "smart", and immune interactions.
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http://dx.doi.org/10.1021/acs.molpharmaceut.0c00287 | DOI Listing |
J Infect Dev Ctries
December 2024
Division of Pulmonary and Critical Care Medicine, Department of Medicine, Faculty of Medicine, Thammasat University, Pathumthani 12120, Thailand.
Introduction: Coronavirus disease 2019 (COVID-19) is associated with long-term symptoms, but the spectrum of these symptoms remains unclear. We aimed to identify the prevalence and factors associated with persistent symptoms in patients at the post-COVID-19 outpatient clinic.
Methodology: This cross-sectional, observational study included hospitalized severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infected patients followed-up at a post-COVID-19 clinic between September 2021 and January 2022.
Objective: To explore the lived experiences and extent of cognitive symptoms in Long COVID (LC) in a UK-based sample.
Design: This study implemented a mixed-methods design. Eight focus groups were conducted to collect qualitative data, and the Framework Analysis was used to reveal the experiences and impact of cognitive symptoms.
Ischemic stroke can cause damage to neurons, resulting in neurological dysfunction. The main treatments in the acute phase include intravenous thrombolysis, endovascular stent-assisted vascular thrombectomy and antiplatelet therapy. Due to the limitations of the time window and the risk of early intracranial hemorrhage, finding active treatment plans is crucial for improving therapy.
View Article and Find Full Text PDFJ Psychiatr Res
January 2025
Department of Molecular Cell Biology, Institute for Cancer Research, Oslo University Hospital, 0379, Oslo, Norway; Centre for Cancer Cell Reprogramming, Faculty of Medicine, University of Oslo, Oslo, Norway; Department for Mechanical, Electronics and Chemical Engineering, Oslo Metropolitan University, Oslo, Norway.
Biomarkers for the diagnosis and clinical management of psychiatric disorders are currently lacking. Extracellular vesicles (EVs), lipid membrane-encapsulated vesicles released by cells, hold promise as a source of biomarkers due to their ability to carry molecules that reflect the status of their donor cells and their ubiquitous presence in biofluids. This review examines the literature on EVs in biofluids from psychiatric disorder patients, and discuss how the published studies contribute to our understanding of the pathophysiology of these conditions and to the discovery of potential biomarkers.
View Article and Find Full Text PDFJ Cereb Blood Flow Metab
January 2025
Neurovascular Research Laboratory, Faculty of Life Sciences and Education, University of South Wales, Pontypridd, UK.
To what extent sildenafil, a selective inhibitor of the type-5 phosphodiesterase modulates systemic redox status and cerebrovascular function during acute exposure to hypoxia remains unknown. To address this, 12 healthy males (aged 24 ± 3 y) participated in a randomized, placebo-controlled crossover study involving exposure to both normoxia and acute (60 min) hypoxia (Fi = 0.14), followed by oral administration of 50 mg sildenafil and placebo (double-blinded).
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