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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]

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]

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]

Titanium implants have revolutionized restorative and reconstructive therapy, yet achieving optimal osseointegration and ensuring long-term implant success remain persistent challenges. In this review, we explore a cutting-edge approach to enhancing implant properties: ultraviolet (UV) photofunctionalization. By harnessing UV energy, photofunctionalization rejuvenates aging implants, leveraging and often surpassing the intrinsic potential of titanium materials. The primary aim of this narrative review is to offer an updated perspective on the advancements made in the field, providing a comprehensive overview of recent findings and exploring the relationship between UV-induced physicochemical alterations and cellular responses. There is now compelling evidence of significant transformations in titanium surface chemistry induced by photofunctionalization, transitioning from hydrocarbon-rich to carbon pellicle-free surfaces, generating superhydrophilic surfaces, and modulating the electrostatic properties. These changes are closely associated with improved cellular attachment, spreading, proliferation, differentiation, and, ultimately, osseointegration. Additionally, we discuss clinical studies demonstrating the efficacy of UV photofunctionalization in accelerating and enhancing the osseointegration of dental implants. Furthermore, we delve into recent advancements, including the development of one-minute vacuum UV (VUV) photofunctionalization, which addresses the limitations of conventional UV methods as well as the newly discovered functions of photofunctionalization in modulating soft tissue and bacterial interfaces. By elucidating the intricate relationship between surface science and biology, this body of research lays the groundwork for innovative strategies aimed at enhancing the clinical performance of titanium implants, marking a new era in implantology.

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., (© The Author(s) (2021). Published by Oxford University Press on behalf of the Guarantors of Brain. All rights reserved. For permissions, please email: journals.permissions@oup.com.)

Hepatocyte growth factor (HGF) and its receptor, cMET, play critical roles in cell proliferation, angiogenesis and invasion in a wide variety of cancers. We therefore examined the anti-tumor activity of the humanized monoclonal anti-HGF antibody, YYB-101, in nude mice bearing human glioblastoma xenografts as a single agent or in combination with temozolomide. HGF neutralization, The extracellular signal-related kinases 1 and 2 (ERK1/2) phosphorylation, and HGF-induced scattering were assessed in HGF-expressing cell lines treated with YYB-101. To support clinical development, we also evaluated the preclinical pharmacokinetics and toxicokinetics in cynomolgus monkeys, and human and cynomolgus monkey tissue was stained with YYB-101 to test tissue cross-reactivity. We found that YYB-101 inhibited cMET activation in vitro and suppressed tumor growth in the orthotopic mouse model of human glioblastoma. Combination treatment with YYB-101 and temozolomide decreased tumor growth and increased overall survival compared with the effects of either agent alone. Five cancer-related genes (TMEM119, FST, RSPO3, ROS1 and NBL1) were overexpressed in YYB-101-treated mice that showed tumor regrowth. In the tissue cross-reactivity assay, critical cross-reactivity was not observed. The terminal elimination half-life was 21.7 days. Taken together, the in vitro and in vivo data demonstrated the anti-tumor efficacy of YYB-101, which appeared to be mediated by blocking the HGF/cMET interaction. The preclinical pharmacokinetics, toxicokinetics and tissue cross-reactivity data support the clinical development of YYB-101 for advanced cancer.

Purpose: We aimed to investigate the effectiveness of ferritin as a contrast agent and a potential reporter gene for tracking tumor cells or macrophages in mouse cancer models., Materials and Methods: Adenoviral human ferritin heavy chain (Ad-hFTH) was administrated to orthotopic glioma models and subcutaneous colon cancer mouse models using U87MG and HCT116 cells, respectively. Brain MR images were acquired before and daily for up to 6 days after the intracranial injection of Ad-hFTH. In the HCT116 tumor model, MR examinations were performed before and at 6, 24, and 48 h after intratumoral injection of Ad-hFTH, as well as before and every two days after intravenous injection of ferritin-labeled macrophages. The contrast effect of ferritin in vitro was measured by MR imaging of cell pellets. MRI examinations using a 7T MR scanner comprised a T1-weighted (T1w) spin-echo sequence, T2-weighted (T2w) relaxation enhancement sequence, and T2*-weighted (T2*w) fast low angle shot sequence., Results: Cell pellet imaging of Ad-hFTH in vitro showed a strong negatively enhanced contrast in T2w and T2*w images, presenting with darker signal intensity in high concentrations of Fe. T2w images of glioma and subcutaneous HCT116 tumor models showed a dark signal intensity around or within the Ad-hFTH tumor, which was distinct with time and apparent in T2*w images. After injection of ferritin-labeled macrophages, negative contrast enhancement was identified within the tumor., Conclusion: Ferritin could be a good candidate as an endogenous MR contrast agent and a potential reporter gene that is capable of maintaining cell labeling stability and cellular safety., Competing Interests: The authors have no financial conflicts of interest.

Glioma stemness has been recognized as the most important reason for glioma relapse and drug resistance. Differentiation of glioma stem cells (GSCs) has been implicated as a novel approach to target recurrent glioma. However, the detailed molecular mechanism involved in the differentiation of GSCs has not yet been elucidated. This study identified CPEB1 as the key modulator that induces the differentiation of GSCs at the post-transcriptional level. Gain and loss of function experiments showed that CPEB1 expression reduced sphere formation ability and the expression of stemness markers such as Nestin and Notch. To elucidate the detailed molecular mechanism underlying the action of CPEB1, we investigated the interacting ribonome of the CPEB1 complex using a Ribonomics approach. CPEB1 specifically suppressed the translation of HES1 and SIRT1 by interacting with a cytoplasmic polyadenylation element. The expression profile of CPEB1 negatively correlated with overall survival in glioma patients. Overexpression of CPEB1 decreased the number of GSCs in an orthotopically implanted glioma animal model. These results suggest that CPEB1-mediated translational control is essential for the differentiation of GSCs and provides novel therapeutic concepts for differentiation therapy.