Data_Sheet_1_Research hotspots and frontiers in post-stroke dysphagia: a bibliometric analysis study.pdf

BackgroundDysphagia is a common complication of stroke that can result in serious consequences. In recent years, more and more papers on post-stroke dysphagia have been published in various journals. However, there is still a lack of bibliometric analysis of post-stroke dysphagia. This study visually analyzes the global research situation of post-stroke dysphagia from 2013 to 2022, aiming to explore the current research status, frontier trends, and research hotspots in this field.MethodsArticles and reviews relevant to post-stroke dysphagia were obtained and retrieved from the Web of Science core collection database in the last 10 years (from 2013 to 2022). CiteSpace and Microsoft Excel 2019 were used for bibliographic analysis.ResultsA total of 1,447 articles were included in the analysis. The number of publications showed an overall upward trend, from 72 in 2013 to 262 in 2022. The most influential authors, institutions, journals, and countries were Hamdy S, University of London, Dysphagia, and the People's Republic of China. An analysis of keywords and the literature indicated that current studies in the field of post-stroke dysphagia focused on dysphagia and aspiration, dysphagia classification, dysphagia rehabilitation, and daily living.ConclusionThis bibliometric analysis reveals the latest advancements and emerging trends in the field of post-stroke dysphagia, spanning the years 2013 to 2022. It highlights the paramount importance of conducting large-scale randomized controlled trials examining the efficacy of dysphagia screening protocols and non-invasive intervention techniques in improving the quality of life for these patients. Such research efforts hold significant academic implications for the development of evidence-based treatment strategies in this field.</p

An Herpesvirus Virulence Factor Inhibits Dendritic Cell Activation Through Protein Phosphatase 1 and IκB Kinase

Dendritic cells are sentinels in innate and adaptive immunity. Upon virus infection, a complex program is in operation, which activates I kappa B kinase (IKK), a key regulator of inflammatory cytokines and costimulatory molecules. Here we show that the gamma(1)34.5 protein, a virulence factor of herpes simplex viruses, blocks Toll-like receptor-mediated dendritic cell maturation. While the wild-type virus inhibits the induction of major histocompatibility complex (MHC) class II, CD86, interleukin-6 (IL-6), and IL-12, the gamma(1)34.5-null mutant does not. Notably, gamma(1)34.5 works in the absence of any other viral proteins. When expressed in mammalian cells, including dendritic cells, gamma(1)34.5 associates with IKK alpha/beta and inhibits NF-kappa B activation. This is mirrored by the inhibition of IKK alpha/beta phosphorylation, p65/RelA phosphorylation, and nuclear translocation in response to lipopolysaccharide or poly(I:C) stimulation. Importantly, gamma(1)34.5 recruits both IKK alpha/beta and protein phosphatase 1, forming a complex that dephosphorylates two serine residues within the catalytic domains of I kappa B kinase. The amino-terminal domain of gamma(1)34.5 interacts with IKK alpha/beta, whereas the carboxyl-terminal domain binds to protein phosphatase 1. Deletions or mutations in either domain abolish the activity of gamma(1)34.5. These results suggest that the control of I kappa B kinase dephosphorylation by gamma(1)34.5 represents a critical viral mechanism to disrupt dendritic cell functions

Tuning of Interlayer Interaction in MoS₂–WS₂ van der Waals Heterostructures Using Hydrostatic Pressure

Van der Waals heterostructures have recently attracted great interest of the scientific community due to their rich exotic physical properties and extensive application prospects. Therefore, we conducted pressure-dependent Raman and photoluminescence spectroscopic studies on MoS2–WS2 heterostructures in different twist angles (24.5 and 54°). Thus, it was confirmed that as the interlayer interaction increases under pressure, an electronic phase transition and a structural phase transition due to layer sliding are observed at ∼1.8 and ∼3.8 GPa in the HS-24.5° structures, while no phase transition is observed in the HS-54° structures. As a result of a larger tunable interlayer space in HS-24.5° structures, optical properties of HS-24.5° structures are more pressure-sensitive than those of the HS-54° structure. It is expected that this work will help comprehensively establish the correlation between the interlayer interactions and optical properties of vdW HSs at the atomic level. Understanding this correlation is crucial for the development of new excitonic devices