Knowledge Structure and Emerging Trends of Mild Cognitive Impairment with Dyssomnias in Recent 20 Years: A Bibliometric Analysis via CiteSpace and VOSviewer.

Background: Mild cognitive impairment (MCI), an intermediate stage between normal aging and dementia, has emerged as a prominent research area in geriatric care due to its heightened propensity for progressing toward dementia. Sleep plays a pivotal role in cognitive function, with dyssomnias not only exacerbating cognitive and affective symptoms associated with neurodegenerative diseases but also contributing to disease progression. Aim: This bibliometric analysis investigates the global research on MCI with dyssomnias over the past two decades, aiming to discern key findings, research domains, and emerging trends in this field. Methods: In this study, a bibliometric analysis was conducted using the search terms "MCI" and "sleep". Data were extracted from the Web of Science Core Collection database, and visualization and collaborative analysis were performed using CiteSpace and VOSviewer. Results: This study encompassed 546 publications from 2003 to 2023. The publication volume and citation rate consistently increased over time. Neurosciences, Clinical Neurology, and Geriatrics Gerontology emerged as the top three research fields. The Journal of Alzheimer's Disease had the highest publication count, while Sleep Medicine received the most citations. USA, China, and Italy led in publication output. Collaborative clusters among authors and institutions were identified, but cooperation between clusters was limited. Active cocited reference clusters included "obstructive sleep apnea", "possible mediating pathways", and "isolated rapid eye movement sleep behaviour disorder". The top frequently mentioned keywords, besides "MCI", were "Alzheimer's disease", "dementia", "risk factor", and "Parkinson's Disease". Notable keyword clusters spanned circadian rhythm, Parkinson's disease, MCI, dementia with Lewy body, subjective cognitive impairment, Lewy body disease, Alzheimer's disease, and dietary patterns. Conclusion: The field of MCI with dyssomnias is rapidly expanding, encompassing a wide range of neurodegenerative disorders and sleep disturbances. Current research endeavors are primarily focused on elucidating the underlying pathogenesis, predicting disease progression, and developing innovative treatment strategies for individuals affected by MCI with dyssomnias.

Utilizing fNIRS to investigate the impact of Baduanjin training on attentional function in post-stroke cognitive impairment patients: a study protocol for a randomized controlled trial.

BACKGROUND: Post-stroke cognitive impairment (PSCI) is a prevalent complication among stroke survivors. It not only directly impacts patients' cognitive abilities but also hampers their capacity to regain independence in daily activities, consequently diminishing their quality of life. Among the various cognitive deficits following stroke, impaired attention is the most frequently observed, influencing not only daily functioning but also higher cognitive functions like working memory, executive functioning, and language.Emerging evidence indicates that Baduanjin, a traditional Chinese exercise, may have a positive impact on enhancing attention in older adults with mild cognitive impairment and stroke survivors. However, the precise mechanisms behind this effect remain unclear. In this study, we employed Baduanjin training as an intervention to address attention decline in post-stroke cognitive impairment patients and to delve into the potential mechanisms through which Baduanjin training may enhance attention in individuals with PSCI. METHODS: In this prospective randomized controlled trial, we plan to recruit 72 participants diagnosed with post-stroke cognitive impairment (PSCI). These participants will be randomly assigned in a 1:1:1 ratio to one of three groups: Baduanjin training(left hemisphere stroke and right hemisphere stroke) and conventional treatment.The conventional treatment group will receive standard rehabilitation sessions. In addition to conventional treatment, participants in the octogenarian training groups will undergo octogenarian training sessions lasting 40 min, five times a week, over a total period of 12 weeks.The primary outcome measures will include the Montreal Cognitive Assessment (MoCA) scale and the Attentional Lateralization Index. These assessments will be conducted by a trained evaluator before the start of the intervention and at weeks 6 and 12 after the intervention begins.Secondary outcome measures will be assessed using the baseline Mandarin version of the Oxford Cognitive Screening (OCS-P) scale, the simplified Fugl-Meyer Motor Function Assessment (FMA) scale, the Pittsburgh Rehabilitation Participation (PRPS) scale, and the Activities of Daily Living (ADL) scale before and after the intervention, respectively. DISCUSSION: This trial aims to examine the impact of Baduanjin training on attentional lateralization among patients with post-stroke cognitive impairment (PSCI). Functional brain imaging utilizing near-infrared spectroscopy will be employed to investigate how Baduanjin exercise influences the structural and functional connectivity of distinct brain regions or brain networks. TRIAL REGISTRATION: Chictr.org.cn, ID: ChiCTR2300076533 . Registered on 11 October 2023.

Nrf2 regulates the expression of NOX1 in TNF-α-induced A549 cells.

Acute lung injury causes severe inflammation and oxidative stress in lung tissues. In this study, we analyzed the potential regulatory role of nuclear factor erythroid-2-related factor 2 (Nrf2) on NADPH oxidase 1 (NOX1) in tumor necrosis factor-α (TNF-α)-induced inflammation and oxidative stress in human type II alveolar epithelial cells. In this study, A549 cells were transfected with Nrf2 siRNA and overexpression vectors for 6 h before being induced by TNF-α for 24 h. TNF-α upregulated the expression of NOX1 and Nrf2 in A549 cells. Furthermore, overexpression of Nrf2 could reduce TNF-α-induced NF-κB mRNA and protein expression after transfection with the Nrf2 siRNA vector, and the levels of IL-6, IL-8, ROS, and malondialdehyde (MDA) in TNF-α-induced A549 cells increased, while the level of total antioxidation capability (T-AOC) decreased. On the other hand, the overexpression of Nrf2 decreased the levels of IL-6, IL-8, ROS, and MDA, while increasing T-AOC. The mRNA and protein levels of NOX1 were dramatically increased by TNF-α, while those changes were notably suppressed by Nrf2 overexpression. Further studies demonstrated that Nrf2 suppressed NOX1 transcription by binding to the -1199 to -1189 bp (ATTACACAGCA) region of the NOX1 promoter in TNF-α-stimulated A549 cells. Our study suggests that Nrf2 may bind to and regulate NOX1 expression to antagonize TNF-α-induced inflammatory reaction and oxidative stress in A549 cells.

Nrf2 regulates the expression of NOX1 in TNF-a-induced A549 cells

Acute lung injury causes severe inflammation and oxidative stress in lung tissues. In this study, we analyzed the potential regulatory role of nuclear factor erythroid-2-related factor 2 (Nrf2) on NADPH oxidase 1 (NOX1) in tumor necrosis factor-α (TNF-α)-induced inflammation and oxidative stress in human type II alveolar epithelial cells. In this study, A549 cells were transfected with Nrf2 siRNA and overexpression vectors for 6 h before being induced by TNF-α for 24 h. TNF-α upregulated the expression of NOX1 and Nrf2 in A549 cells. Furthermore, overexpression of Nrf2 could reduce TNF-α-induced NF-κB mRNA and protein expression after transfection with the Nrf2 siRNA vector, and the levels of IL-6, IL-8, ROS, and malondialdehyde (MDA) in TNF-α-induced A549 cells increased, while the level of total antioxidation capability (T-AOC) decreased. On the other hand, the overexpression of Nrf2 decreased the levels of IL-6, IL-8, ROS, and MDA, while increasing T-AOC. The mRNA and protein levels of NOX1 were dramatically increased by TNF-α, while those changes were notably suppressed by Nrf2 overexpression. Further studies demonstrated that Nrf2 suppressed NOX1 transcription by binding to the -1199 to -1189 bp (ATTACACAGCA) region of the NOX1 promoter in TNF-α-stimulated A549 cells. Our study suggests that Nrf2 may bind to and regulate NOX1 expression to antagonize TNF-α-induced inflammatory reaction and oxidative stress in A549 cells (AU)

Large mediastinal mass diagnosed as Nocardia infection by endobronchial ultrasound-guided transbronchial needle aspiration in a ceramic worker: A case report.

Background: Nocardia is a ubiquitous soil saprophyte transmitted through airborne or direct cutaneous inoculation routes. Although Nocardia is more common in immunocompromised patients, Nocardia may also arise in apparently immunocompetent patients. Case presentation: We report a rare case of Nocardia infection presenting as a large mediastinal mass in an immunocompetent ceramic worker. A 54-year-old man with no previous history of immune dysfunction, a ceramic worker by profession, was referred and admitted to our hospital because of a persistent fever for 19 days. Chest CT showed a large middle mediastinal mass. However, conventional anti-infective treatment was ineffective. Under the guidance of the Virtual bronchoscopic navigation (VBN) system, he underwent Endobronchial ultrasound-guided transbronchial needle aspiration (EBUS-TBNA). The purulent exudate obtained by EBUS-TBNA was further identified as Nocardia by weak acid-fast and metagenomic next-generation sequencing (mNGS). He was subsequently treated with intravenous imipenem/amikacin, switched to intravenous imipenem and oral trimethoprim/sulfamethoxazole, and the clinical symptoms were significantly improved. Conclusions: Even in immunocompetent patients, Nocardiosis cannot be excluded. For the public, especially soil contact workers, precautions should be taken to avoid Nocardia infection from occupational exposure. This rare case may provide a diagnosis and treatment reference for clinicians.

Nuclear factor-kappaB regulates the transcription of NADPH oxidase 1 in human alveolar epithelial cells.

OBJECTIVE: Acute lung injury (ALI) is characterized by inflammation and oxidative stress. Nuclear factor-kappaB (NF-κB) mediates the expression of various inflammation-related genes, including the NADPH oxidase family. This study aimed to identify the potential regulatory role of NF-κB on NADPH oxidases in tumor necrosis factor-α (TNF-α)-induced oxidative stress in human alveolar epithelial cells. METHODS: A549 cells were treated with TNF-α for 24 h to establish ALI cell models. RT-PCR, western blot, assessment of oxidative stress, Alibaba 2.1 online analysis, electrophoretic mobility shift assays and luciferase reporter analysis were employed to identify the potential regulatory role of NF-κB on NADPH oxidases in TNF-α-induced oxidative stress in human alveolar epithelial cells. RESULTS: The expression of NF-κB/p65 was notably upregulated in TNF-α-stimulated A549 cells. NF-κB knockdown by siRNA significantly inhibited the TNF-α-induced oxidative stress. Moreover, NF-κB/p65 siRNA could inhibit the activation of NOX1, NOX2 and NOX4 mRNA and protein expression in TNF-α-stimulated A549 cells. The next study demonstrated that NF-κB activated the transcription of NOX1 by binding to the -261 to -252 bp (NOX1/κB2, TAAAAATCCC) region of NOX1 promoter in TNF-α-stimulated A549 cells. CONCLUSION: Our data demonstrated that NF-κB can aggravate TNF-α-induced ALI by regulating the oxidative stress response and the expression of NOX1, NOX2 and NOX4. Moreover, NF-κB could promote the NOX1 transcriptional activity via binding its promoter in TNF-α-stimulated A549 cells.