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Considering the biological activity of osteoblasts is crucial when devising new approaches to enhance the osseointegration of implant surfaces, as their behavior profoundly influences clinical outcomes. An established inverse correlation exists between osteoblast proliferation and their functional differentiation, which constrains the rapid generation of a significant amount of bone. Examining the surface morphology of implants reveals that roughened titanium surfaces facilitate rapid but thin bone formation, whereas smooth, machined surfaces promote greater volumes of bone formation albeit at a slower pace. Consequently, osteoblasts differentiate faster on roughened surfaces but at the expense of proliferation speed. Moreover, the attachment and initial spreading behavior of osteoblasts are notably compromised on microrough surfaces. This review delves into our current understanding and recent advances in nanonodular texturing, meso-scale texturing, and UV photofunctionalization as potential strategies to address the "biological dilemma" of osteoblast kinetics, aiming to improve the quality and quantity of osseointegration. We discuss how these topographical and physicochemical strategies effectively mitigate and even overcome the dichotomy of osteoblast behavior and the biological challenges posed by microrough surfaces. Indeed, surfaces modified with these strategies exhibit enhanced recruitment, attachment, spread, and proliferation of osteoblasts compared to smooth surfaces, while maintaining or amplifying the inherent advantage of cell differentiation. These technology platforms suggest promising avenues for the development of future implants. [ABSTRACT FROM AUTHOR]

Trichospira verticillata is an annual herb that belongs to the family Asteraceae. Trichospira verticillata extract (TVE) elicits anti‐plasmodial activity; however, there has been no detailed report about its anti‐inflammatory effects and molecular mechanisms. In addition, herbal plants exhibit anti‐inflammatory effects by suppressing the NLRP3 inflammasome. Therefore, the primary goal of this study was to examine the effects of TVE on NLRP3 inflammasome activation by measuring interleukin‐1β (IL‐1β) secretion. We treated lipopolysaccharides (LPS)‐primed J774A.1 and THP‐1 cells with TVE, which attenuated NLRP3 inflammasome activation. Notably, TVE did not affect nuclear factor‐kappa B (NF‐κB) signalling or intracellular reactive oxygen species (ROS) production and potassium efflux, suggesting that it inactivates the NLRP3 inflammasome via other mechanisms. Moreover, TVE suppressed the formation of apoptosis‐associated speck‐like protein (ASC) speck and oligomerization. Immunoprecipitation data revealed that TVE reduced the binding of NLRP3 to NIMA‐related kinase 7 (NEK7), resulting in reduced ASC oligomerization and speck formation. Moreover, TVE alleviated neutrophilic asthma (NA) symptoms in mice. This study demonstrates that TVE modulates the binding of NLPR3 to NEK7, thereby reporting novel insights into the mechanism by which TVE inhibits NLRP3 inflammasome. These findings suggest TVE as a potential therapeutic of NLRP3 inflammasome‐mediated diseases, particularly NA. [ABSTRACT FROM AUTHOR]

Human‐induced climate change causes extreme weather events, and flooding induced by heavy rainfall in the riparian system is no exception. The southern Korean Peninsula witnessed record‐breaking rainfall during the summer of 2020, resulting in an extreme flood event that caused extensive damage to the riparian ecosystem along the Seomjin River. This study was aimed at identifying the composite factors of riparian vegetation destruction along the entire river. Based on a spatially explicit multilevel approach, it was found that large‐scale geomorphic characteristics (i.e., alternation of plain and valley topographies) appeared to be essential determinants of hydraulic characteristics of the channel (e.g., shear stress and specific energy), which were the leading causes of vegetation destruction. Moreover, at small spatial scales, several trees situated upstream of a vegetation patch protected other plants on the patch from the direct hydraulic impact of the flood, thereby serving as 'shield' trees. These findings indicate that scale‐dependent fluvial biogeomorphic processes take place during extreme flood events; hence, identifying the optimal scales of these processes and associated factors could help in further understanding riparian hydrology from a biogeomorphic point of view. This study suggests that hydrologists consider both geomorphological and ecological factors when studying hydrological processes. [ABSTRACT FROM AUTHOR]

There is still an unmet need for development of safer antimelanogenic or melanin-degrading agents for skin hyperpigmentation, induced by intrinsic or extrinsic factors including aging or ultraviolet irradiation. Owing to the relatively low cytotoxicity compared with other chemical materials, several studies have explored the role of 2'-fucosyllactose (2'-FL), the most dominant component of human milk oligosaccharides. Here, we showed that 2'-FL reduced melanin levels in both melanocytic cells and a human skin equivalent three-dimensional in vitro model. Regarding the cellular and molecular mechanism, 2'-FL induced LC3I conversion into LC3II, an autophagy activation marker, followed by the formation of LC3II+/PMEL+ autophagosomes. Comparative transcriptome analysis provided a comprehensive understanding for the up- and downstream cellular processes and signaling pathways of the AMPK–ULK1 signaling axis triggered by 2'-FL treatment. Moreover, 2'-FL activated the phosphorylation of AMPK at Thr172 and of ULK1 at Ser555, which were readily reversed in the presence of dorsomorphin, a specific AMPK inhibitor, with consequent reduction of the 2'-FL-mediated hypopigmentation. Taken together, these findings demonstrate that 2'-FL promotes melanin degradation by inducing autophagy through the AMPK–ULK1 axis. Hence, 2'-FL may represent a new natural melanin-degrading agent for hyperpigmentation. [ABSTRACT FROM AUTHOR]

Gait, the style of human walking, has been studied as a behavioral characteristic of an individual. Several studies have utilized gait to identify individuals with the aid of machine learning and computer vision techniques. However, there is a lack of studies on the nature of gait, such as the identification power or the uniqueness. This study aims to quantify the uniqueness of gait in a cohort. Three-dimensional full-body joint kinematics were obtained during normal walking trials from 488 subjects using a motion capture system. The joint angles of the gait cycle were converted into gait vectors. Four gait vectors were obtained from each subject, and all the gait vectors were pooled together. Two gait vectors were randomly selected from the pool and tested if they could be accurately classified if they were from the same person or not. The gait from the cohort was classified with an accuracy of 99.71% using the support vector machine with a radial basis function kernel as a classifier. Gait of a person is as unique as his/her facial motion and finger impedance, but not as unique as fingerprints. [ABSTRACT FROM AUTHOR]

As the clinical failure of glioblastoma treatment is attributed by multiple components, including myelin-associated infiltration, assessment of the molecular mechanisms underlying such process and identification of the infiltrating cells have been the primary objectives in glioblastoma research. Here, we adopted radiogenomic analysis to screen for functionally relevant genes that orchestrate the process of glioma cell infiltration through myelin and promote glioblastoma aggressiveness. The receptor of the Nogo ligand (NgR1) was selected as the top candidate through Differentially Expressed Genes (DEG) and Gene Ontology (GO) enrichment analysis. Gain and loss of function studies on NgR1 elucidated its underlying molecular importance in suppressing myelin-associated infiltration in vitro and in vivo. The migratory ability of glioblastoma cells on myelin is reversibly modulated by NgR1 during differentiation and dedifferentiation process through deubiquitinating activity of USP1, which inhibits the degradation of ID1 to downregulate NgR1 expression. Furthermore, pimozide, a well-known antipsychotic drug, upregulates NgR1 by post-translational targeting of USP1, which sensitizes glioma stem cells to myelin inhibition and suppresses myelin-associated infiltration in vivo. In primary human glioblastoma, downregulation of NgR1 expression is associated with highly infiltrative characteristics and poor survival. Together, our findings reveal that loss of NgR1 drives myelin-associated infiltration of glioblastoma and suggest that novel therapeutic strategies aimed at reactivating expression of NgR1 will improve the clinical outcome of glioblastoma patients. [ABSTRACT FROM AUTHOR]

Background: Botulinum toxin (BoNT) is widely used to treat masseter muscle hypertrophy. Changes in the muscle thickness have been found in many studies, but there has been no report on changes in the thickness from the skin surface to the masseter muscle.Objectives: We aimed to use ultrasonography to measure not only changes in the muscle thickness but also changes in subcutaneous thickness.Methods: This study enrolled 20 volunteer patients: 10 were assigned to an experimental group (injected with each side 25 U of botulinum toxin into both masseter muscles) and 10 to a control group (injected with normal saline). The thicknesses were measured before the injection and at 4, 8, and 12 weeks after the injection both at rest and during maximum muscle contraction.Results: The subcutaneous thickness did not differ significantly over time either at rest (P = 0.063) or during maximal contraction (P = 0.392), or between the experimental and control groups at rest (P = 0.392) or during maximum contraction (P = 0.259). The muscle thickness in the experimental group differed significantly over time.Conclusions: Botulinum toxin injection only changes the muscle thickness and does not affect the subcutaneous thickness from the skin surface to the masseter muscle. [ABSTRACT FROM AUTHOR]

Corrections to the article "Pigment Epithelium-Derived Factor (PEDF) Expression Induced by EGFRvIII Promotes Self-renewal and Tumor Progression of Glioma Stem Cells" are presented.

A 16.8 Gbps/channel single-ended transceiver for SiP-based DRAM interface on silicon carrier channel is proposed in this paper. A transmitter, receiver, and channel are all included in a single package as SiP. A current mode 4:1 MUX with 1-tap feed-forward equalizer (FFE) is used as a serializer, and this 4:1 MUX uses 25% duty clock to prevent short circuit current when consecutive 2-phase clocks overlap. Additionally, an open drain output driver with asynchronous type 1-tap FFE is used in the transmitter. Because of its small physical size, a common mode variation of Si-carrier channel from process variation is more serious than that of conventional PCB. This common mode variation degrades bit error rates (BER) at single-ended signaling. To obtain effective single-ended signaling on Si-carrier channel, a source follower-based continuous time linear equalizers and self-VREF generator with training algorithm on the receiver are proposed. An implemented Si-carrier channel uses meshed layer as a reference to reduce insertion loss. A BER less than 1e-12 is achieved in 65 nm CMOS and the power efficiency of the transceiver is 5.9 pJ/bit with 120 \Omega terminations at each transceiver side. [ABSTRACT FROM PUBLISHER]

These authors contributed equally: Hyojin Heo, Byungsun Cha and Dongmin Jang. "These authors contributed equally: Hyojin Heo and Byungsun Cha". now reads: "These authors contributed equally: Hyojin Heo, Byungsun Cha and Dongmin Jang". Author Correction: Human milk oligosaccharide 2'-fucosyllactose promotes melanin degradation via the autophagic AMPK-ULK1 signaling axis. [Extracted from the article]

Epidermal growth factor receptor variant III (EGFRvIII) has been associated with glioma stemness, but the direct molecular mechanism linking the two is largely unknown. Here, we show that EGFRvIII induces the expression and secretion of pigment epithelium-derived factor (PEDF) via activation of signal transducer and activator of transcription 3 (STAT3), thereby promoting self-renewal and tumor progression of glioma stem cells (GSCs). Mechanistically, PEDF sustained GSC self-renewal by Notch1 cleavage, and the generated intracellular domain of Notch1 (NICD) induced the expression of Sox2 through interaction with its promoter region. Furthermore, a subpopulation with high levels of PEDF was capable of infiltration along corpus callosum. Inhibition of PEDF diminished GSC self-renewal and increased survival of orthotopic tumor-bearing mice. Together, these data indicate the novel role of PEDF as a key regulator of GSC and suggest clinical implications. [ABSTRACT FROM AUTHOR]