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Background: The vestibular system not only supports reflex function at the brainstem level, but is also associated with higher levels of cognitive function. Vertigo due to vestibular disorders may lead to or be associated with cognitive dysfunction. Patients with deficits of both vestibular as well as cognitive function may be at particularly high risk for events like falls or certain diseases, such as Alzheimer's. Objective: To analyze the current state of research and trends in the global research literature regarding the correlation between vestibular disorders, vertigo, and cognitive impairment. Methods: We utilized Bibliometrix package to search databases including PubMed, Web of Science, etc for search terms. Results: Databases were searched up to December 15, 2022, and a total of 2222 publications were retrieved. Ultimately, 53 studies were included. A total of 261 authors published in 38 journals and conferences with an overall increasing annual growth rate of 6.94%. The most-published journal was Frontiers in Neurology . The most-published country was the United States, followed by Italy and Brazil. The most-published institution was Johns Hopkins University with a total of 13 articles. On performing trend analysis, we found that the most frequent focus of research in this field include the testing of vestibular perception, activation of the brain-related cortex, and the influence of stimulus-triggered vestibular snail reflex on visual space. The potential focal points are the risk of falling and the ability to extract spatial memory information, and the focus of research in recent decades has revolved around balance, falling, and Alzheimer's disease. Conclusions: Vestibular impairment in older adults affects cognitive function, particularly immediate memory, visuospatial cognition, and attention, with spatial cognition being the most significantly affected. In the future, virtual reality-based vestibular rehabilitation techniques and caloric stimulation could be potential interventions for the treatment of cognitive impairment., Competing Interests: Declaration of Conflicting InterestsThe author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Objectives: To investigate the role of m.4435A>G and YARS2 c.572G>T (p.G191V) mutations in the development of essential hypertension., Methods: A hypertensive patient with m.4435A>G and YARS2 p.G191V mutations was identified from previously collected mitochondrial genome and exon sequencing data. Clinical data were collected, and a molecular genetic study was conducted in the proband and his family members. Peripheral venous blood was collected, and immortalized lymphocyte lines constructed. The mitochondrial transfer RNA (tRNA), mitochondrial protein, adenosine triphosphate (ATP), mitochondrial membrane potential (MMP), and reactive oxygen species (ROS) in the constructed lymphocyte cell lines were measured., Results: Mitochondrial genome sequencing showed that all maternal members carried a highly conserved m.4435A>G mutation. The m.4435A>G mutation might affect the secondary structure and folding free energy of mitochondrial tRNA and change its stability, which may influence the anticodon ring structure. Compared with the control group, the cell lines carrying m.4435A>G and YARS2 p.G191V mutations had decreased mitochondrial tRNA homeostasis, mitochondrial protein expression, ATP production and MMP levels, as well as increased ROS levels (all P <0.05)., Conclusions: The YARS2 p.G191V mutation aggravates the changes in mitochondrial translation and mitochondrial function caused by m.4435A>G through affecting the steady-state level of mitochondrial tRNA and further leads to cell dysfunction, indicating that YARS2 p.G191V and m.4435A>G mutations have a synergistic effect in this family and jointly participate in the occurrence and development of essential hypertension.

Background: Adipose tissue engineering plays a key role in the reconstruction of soft-tissue defects. The acellular adipose matrix (AAM) is a promising biomaterial for the construction of engineered adipose tissue. However, AAM lacks sufficient adipoinduction potency because of the abundant loss of matrix-bound adipokines during decellularization., Methods: An adipose-derived extracellular matrix collagen scaffold, "adipose collagen fragment" (ACF), was prepared using a novel mechanical method that provides sustained release of adipokines. Here, the authors used label-free proteomics methods to detect the protein components in AAM and ACF. In vivo, ACF was incorporated into AAM or acellular dermal matrix and implanted into nude mice to evaluate adipogenesis. Neoadipocytes, neovessels, and corresponding gene expression were evaluated. The effects of ACF on adipogenic differentiation of human adipose-derived stem cells and tube formation by human umbilical vein endothelial cells were tested in vitro., Results: Proteomics analysis showed that ACF contains diverse adipogenic and angiogenic proteins. ACF can release diverse adipokines and induce highly vascularized, mature adipose tissue in AAM, and even in nonadipogenic acellular dermal matrix. Higher expression of adipogenic markers peroxisome proliferator-activated receptor gamma and CCAAT/enhancer-binding protein alpha and greater numbers of tubule structures were observed in ACF-treated groups in vitro., Conclusion: The combination of ACF and AAM could serve as a novel and promising strategy to construct mature, vascularized adipose tissue for soft-tissue reconstruction., Clinical Relevance Statement: The combined use of AAM and ACF has been proven to induce a highly vascularized, mature, engineered adipose tissue in the nude mouse model, which may serve as a promising strategy for soft-tissue reconstruction., (Copyright © 2023 by the American Society of Plastic Surgeons.)