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Background: Thousands of people with multiple sclerosis (MS) have used self-administered oxygen therapy in the UK. Clinical trials have been performed, with scant evidence that people with MS have been consulted to explore how they benefit from or how to optimize this treatment. The conventional MS disease disability scores used in trials seldom reflect the effects individuals report when using oxygen therapy to treat their symptoms.
Methods: Three people with MS and the manager of an MS Centre formed a public involvement group and collaborated with clinicians and scientists to inform a lab-based study to investigate the physiological effects of oxygen therapy on microvascular brain endothelial cells.
Results: People with MS often use oxygen therapy at a later stage when their symptoms worsen and only after using other treatments. The frequency of oxygen therapy sessions and hyperbaric pressure is individualized and varies for people with MS. Despite direct comparisons of efficacy proving difficult, most individuals are exposed to 100% O at 1.5 atmosphere absolute (ATA; 1140 mmHg absolute) for 60 min. In a laboratory-based study human brain endothelial cells were exposed in vitro to 152 mmHg O for 60 min with and without pressure, as this equates to 20% O achievable via hyperbarics, which was then replicated at atmospheric pressure. A significant reduction in endothelial cells ICAM-1 (CD54) implicated in inflammatory cell margination across the blood brain barrier was observed under oxygen treatment.
Conclusions: By collaborating with people living with MS, we were able to design laboratory-based experimental protocols that replicate their treatment regimens to advance our understanding of the physiological effects of hyperbaric oxygen treatment on brain cells and their role in neuroinflammation.
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http://dx.doi.org/10.1016/j.msard.2020.102084 | DOI Listing |
ACS Appl Bio Mater
September 2025
School of Chemistry and Chemical Engineering, Harbin Institute of Technology, Harbin 150001, China.
The generation of reactive oxygen species (ROS) through nanozyme-mediated sonocatalytic therapy has demonstrated remarkable therapeutic efficacy in the field of cancer. Nevertheless, it remains a significant challenge for nanozymes with a single catalytic active center to generate sufficient ROS via Fenton or Fenton-like reactions to effectively induce tumor cell death. In order to enhance the catalytic efficacy, we devised and synthesized a multiple active centre and mitochondrial-targeted perovskite nanozyme (NCFP), doped with cobalt (Co) element, and incorporated 4-carboxybutyltriphenylphosphonium bromide (TPP) as a mitochondrial targeting marker for ultrasound (US)-assisted enzyme-like catalytic treatment of tumors.
View Article and Find Full Text PDFAnn Am Thorac Soc
September 2025
Brigham and Women's Hospital, Division of Sleep and Circadian Disorders, Boston, Massachusetts, United States.
Rationale: There are insufficient data to inform the management of central sleep apnea (CSA) in patients with heart failure (HF) with reduced ejection fraction (HFrEF). Nocturnal oxygen therapy (NOT) has been postulated to benefit CSA patients with HFrEF, but has not been rigorously studied. This article is open access and distributed under the terms of the Creative Commons Attribution Non-Commercial No Derivatives License 4.
View Article and Find Full Text PDFArq Bras Cardiol
September 2025
Instituto do Coração do Hospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo, São Paulo, SP - Brasil.
Targeted temperature management (TTM) is currently the only potentially neuroprotective intervention recommended for post-cardiac arrest care. However, there are concerns among the scientific community regarding conflicting evidence supporting this recommendation. Moreover, the bulk of trials included in systematic reviews that inform guidelines and recommendations have been conducted in developed countries, with case mix and patient characteristics that significantly differ from the reality of developing countries such as Brazil.
View Article and Find Full Text PDFExp Physiol
September 2025
Department of Hepatobiliary Surgery, The Affiliated Huaian No.1 People's Hospital of Nanjing Medical University, Huaian, Jiangsu, China.
Hepatic ischaemia-reperfusion (IR) injury is a serious clinical issue, especially in patients with type 2 diabetes mellitus (T2DM). As mitochondria play a critical role in the regulation of IR-induced liver damage, mitochondria-targeted treatment is of the utmost significance for improving outcomes. The present study explored the mitoprotective role of combined ginsenoside-MC1 (GMC1) and irisin administration in diabetic rats with hepatic IR injury.
View Article and Find Full Text PDFPLoS One
September 2025
Department of Cardiac Surgery, Faculty of Medicine and University Hospital Cologne, University of Cologne, Cologne, Germany.
Background: Cardiac ischemia reperfusion (I/R) injury is a serious consequence of reperfusion therapy for myocardial infarction (MI). Peptidylarginine deiminase 4 (PAD4) is a calcium-dependent enzyme that catalyzes the citrullination of proteins. In previous studies, PAD4 inhibition protected distinct organs from I/R injury by preventing the formation of neutrophil extracellular traps (NETs) and attenuating inflammatory responses.
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