Feasibility of patient-performed lung ultrasound self-exams (Patient-PLUS) as a potential approach to telemedicine in heart failure.

AIMS: Patient-performed lung ultrasound (LUS) in a heart failure (HF) telemedicine model may be used to monitor worsening pulmonary oedema and to titrate therapy, potentially reducing HF admission. The aim of the study was to assess the feasibility of training HF patients to perform a LUS self-exam in a telemedicine model. METHODS AND RESULTS: A pilot study was conducted at a public hospital involving subjects with a history of HF. After a 15 min training session involving a tutorial video, subjects performed a four-zone LUS using a handheld ultrasound. Exams were saved on a remote server and independently reviewed by two LUS experts. Studies were determined interpretable according to a strict definition: the presence of an intercostal space, and the presence of A-lines, B-lines, or both. Subjects also answered a questionnaire to gather feedback and assess self-efficacy. The median age of 44 subjects was 53 years (range, 36-64). Thirty (68%) were male. Last educational level attained was high school or below for 31 subjects (70%), and one-third used Spanish as their preferred language. One hundred fifty of 175 lung zones (85%) were interpretable, with expert agreement of 87% and a kappa of 0.49. 98% of subjects reported that they could perform this LUS self-exam at home. CONCLUSIONS: This pilot study reports that training HF patients to perform a LUS self-exam is feasible, with reported high self-efficacy. This supports further investigation into a telemedicine model using LUS to reduce emergency department visits and hospitalizations associated with HF.

Glutathione Peroxidase 4 is associated with Neuromelanin in Substantia Nigra and Dystrophic Axons in Putamen of Parkinson's brain.

BACKGROUND: Parkinson's disease is a neurodegenerative disorder characterized pathologically by the loss of nigrostriatal dopamine neurons that project from the substantia nigra in the midbrain to the putamen and caudate nuclei, leading to the clinical features of bradykinesia, rigidity, and rest tremor. Oxidative stress from oxidized dopamine and related compounds may contribute to the degeneration characteristic of this disease. RESULTS: To investigate a possible role of the phospholipid hydroperoxidase glutathione peroxidase 4 (GPX4) in protection from oxidative stress, we investigated GPX4 expression in postmortem human brain tissue from individuals with and without Parkinson's disease. In both control and Parkinson's samples, GPX4 was found in dopaminergic nigral neurons colocalized with neuromelanin. Overall GPX4 was significantly reduced in substantia nigra in Parkinson's vs. control subjects, but was increased relative to the cell density of surviving nigral cells. In putamen, GPX4 was concentrated within dystrophic dopaminergic axons in Parkinson's subjects, although overall levels of GPX4 were not significantly different compared to control putamen. CONCLUSIONS: This study demonstrates an up-regulation of GPX4 in neurons of substantia nigra and association of this protein with dystrophic axons in striatum of Parkinson's brain, indicating a possible neuroprotective role. Additionally, our findings suggest this enzyme may contribute to the production of neuromelanin.

Role of selenoprotein P in Alzheimer's disease.

INTRODUCTION: Selenoprotein P (SelP) plays a critical role in neuronal survival and is associated with Alzheimer's pathology. We sought to determine a potential neuroprotective role for SelP in Alzheimer's disease. METHODS: We utilized RNAi to reduce SelP expression in neuronal N2A cells, and determined cell viability with flow cytometry. We subsequently measured neurotoxicity from exposure of aggregated amyloid beta (Abeta) peptides to SelP-knockdown and control N2A cells. RESULTS: We found that knockdown of SelP using siRNA in N2A cells reduced viability and increased apoptotic cell death. Additionally, knockdown of SelP using siRNA in N2A cells resulted in increased AB toxicity. CONCLUSIONS: Our findings demonstrate that SelP protects neuronal cells from Abeta-induced toxicity, suggesting a neuroprotective role for SelP in preventing neurodegenerative disorders.