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Hypoxia triggers blood-brain barrier disruption and a strong microglial activation response around leaky cerebral blood vessels. These events are greatly amplified in aged mice which is translationally relevant because aged patients are far more likely to suffer hypoxic events from heart or lung disease, and because of the pathogenic role of blood-brain barrier breakdown in vascular dementia. Importantly, it is currently unclear if disrupted cerebral blood vessels spontaneously repair and if they do, whether surrounding microglia deactivates.

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Implantable cardioverter defibrillators (ICDs) are implanted in increasing numbers of patients with the aim of treating ventricular arrhythmias in high-risk patients and reducing their risk of dying. Individuals are also living longer with these devices. As a result, a greater number of patients with an ICD will deteriorate either with worsening cardiac failure, another non-cardiac condition or general frailty and will have a limited prognosis.

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Thiol/disulfide-based redox regulation is a key mechanism for modulating protein functions in response to changes in cellular redox status. Two thioredoxin (Trx)-like proteins [atypical Cys His-rich Trx (ACHT) and Trx-like2 (TrxL2)] have been identified as crucial for oxidizing and deactivating several chloroplast enzymes during light-to-dark transitions; however, their roles remain to be fully understood. In this study, we investigated the functions of Trx-like proteins in seed development.

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