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Emerging RNA viruses such as influenza A virus (IAV), Zika virus (ZIKV), and dengue virus (DENV) continue to pose major challenges to animal and public health due to their high mutation rates, wide host ranges, and immune evasion strategies. In this study, we evaluated the in vitro antiviral activity of a marine bacterial extract derived from Parerythrobacter sp. M20A3S10 against IAV (H1N1; H3N2), influenza B virus (IBV), ZIKV, and DENV2. The extract demonstrated broad-spectrum antiviral effects with favorable selectivity indices across multiple host-derived epithelial cell lines. Notably, post-infection treatment significantly suppressed viral replication, suggesting a host-modulating or replication-inhibiting mechanism. While the extract’s active components have yet to be identified, bacteria from the Erythrobacteraceae family are known producers of bioactive metabolites with potential antiviral properties. These findings provide preliminary insight into the potential of marine-derived bacterial compounds in veterinary antiviral development and highlight the need for further characterization and in vivo validation. This work contributes to the understanding of virus–host interactions and the exploration of novel therapeutic strategies targeting the pathogenesis and immune modulation of veterinary RNA viruses.

CD4 and CD8 T cells are vital components of the immune system. We found that histone deacetylase 3 (HDAC3) is critical for the development of CD4 T cells, as HDAC3-deficient DP thymocytes generate only CD8SP thymocytes in mice. In the absence of HDAC3, MHC Class II-restricted OT-II thymocytes are redirected to the CD8 cytotoxic lineage, which occurs with accelerated kinetics. Analysis of histone acetylation and RNA-seq reveals that HDAC3-deficient DP thymocytes are biased towards the CD8 lineage prior to positive selection. Commitment to the CD4 or CD8 lineage is determined by whether persistent TCR signaling or cytokine signaling predominates, respectively. Despite elevated IL-21R/γc/STAT5 signaling in HDAC3-deficient DP thymocytes, blocking IL-21R does not restore CD4 lineage commitment. Instead, HDAC3 binds directly to CD8-lineage promoting genes. Thus, HDAC3 is required to restrain CD8-lineage genes in DP thymocytes for the generation of CD4 T cells.

Background: To date, Sports Team Smartphone Application (STSA) provides quick information, score, result, and highlights for fans. Also, STSA is a useful marketing tool for professional sports teams in research and practice. Therefore, the purpose of this study is (a) to examine the relationship between information credibility, Technology Acceptance Model (TAM), Intention to Revisit Apps (IRA), and Actual Sport Behavior (ASB) and (b) to apply an integrated Stimulus Organism Response (SOR) framework for the STSA. Method: The sample consisted of 315 participants from four Korean professional baseball teams. Results: The result supported multiple hypotheses. First, information credibility's accuracy and attractiveness significantly influence trustworthiness, perceived ease of use (PEOU), and perceived usefulness (PU). Trustworthiness and attractiveness of information have a positive influence on customers' IRAs. The PEOU influences PU, which affects IRA and ASB. Lastly, IRA significantly influences ASB. This study highlighted the purchasing behavior of sports fans through sports teams' apps. It also provided evidence that sports teams' apps can be beneficial tools to ensure the usefulness of information and IRA. Finally, the data provide evidence that the SOR theory applies to an STSA environment in a sports context. These results suggest that the SOR theory can be used to examine online studies and smartphone apps. Conclusions: Through this study's findings, each sports team's marketers will recognize that sports apps are useful resources to provide information and can be used as mutual communication to attract fans to the teams' apps and games more frequently. Consequently, to maximize sports fans' revisiting of team apps, each team needs to provide accurate, attractive, and useful information. Also, teams must update and monitor their apps constantly for effective management.

NKT cells are a distinct subset that have developmental requirements that often differ from conventional T cells. Here, we show that NKT-specific deletion of Hdac3 results in a severe reduction in the number of iNKT cells, particularly of NKT1 cells. In addition, there is decreased cytokine production by Hdac3-deficient NKT2 and NKT17 cells. Hdac3-deficient iNKT cells have increased cell death that is not rescued by transgenic expression of Bcl-2 or Bcl-xL. Hdac3-deficient iNKT cells have less Cyto-ID staining and lower LC3A/B expression, indicative of reduced autophagy. Interestingly, Hdac3-deficient iNKT cells also have lower expression of the nutrient receptors GLUT1, CD71 and CD98, which would increase the need for autophagy when nutrients are limiting. Therefore, Hdac3 is required for iNKT cell development and differentiation.

iNKT cells are a unique lineage of T cells that recognize glycolipid presented by CD1d. In the thymus, they differentiate into iNKT1, iNKT2 and iNKT17 effector subsets, characterized by preferential expression of Tbet, Gata3 and ROR-γt and production of IFN-γ, IL-4 and IL-17, respectively. We demonstrate that the transcriptional regulator Runx1 is essential for the generation of ROR-γt expressing iNKT17 cells. PLZF-cre Runx1 cKO mice lack iNKT17 cells in the thymus, spleen and liver. Runx1-deficient iNKT cells have altered expression of several genes important for iNKT17 differentiation, including decreased expression of IL-7Rα, BATF and c-Maf and increased expression of Bcl11b and Lef1. However, reduction of Lef1 expression or introduction of an IL-7Rα transgene is not sufficient to correct the defect in iNKT17 differentiation, demonstrating that Runx1 is a key regulator of several genes required for iNKT17 differentiation. Loss of Runx1 leads to a severe decrease in iNKT cell numbers in the thymus, spleen and liver. The decrease in cell number is due to a combined decrease in proliferation at Stage 1 during thymic development and increased apoptosis. Thus, we describe a novel role of Runx1 in iNKT cell development and differentiation, particularly in orchestrating iNKT17 differentiation.

Approximately 58,000 Americans were diagnosed with oral cancer in 2022, and it has a high mortality rate of approximately 47%. 90% of these oral cancer cases have been confirmed to be squamous cell carcinoma, while oral malignant melanoma and adenocarcinomas are less-common types. Part of the reason for the lethality of this disease is late discovery at the advanced stages when diagnosed, showing the importance of identifying tumors or dysplastic cells in the early stages. Due to the high recurrence rate of oral cancer, complete surgical removal of the tumor is required. The current gold standard for the analysis of removed margins is Frozen Section analysis (FS), which is both time-consuming and is limited by significant sampling error. Due to the inability to assess the entire resection margin histologically, proper guidance for the surgical margin of specimen selection is needed. Elastic Scattering Spectroscopy (ESS) is an optical technique that measures backscattered spectra using fiber optics and can detect optical characteristics of the tissue without damaging it. ESS is a point measurement technique, and recent studies in the Bigio lab developed an ESS scanning module that combines an ESS system with a tissue scanning module, enabling a series of measurements in a target area of the tissue, with step sizes of 100 micrometers to 1 mm. However, the current scanning module has drawbacks for practical usage in the clinic: the stability of scanning functions is low; the height of an ESS probe cannot be adjusted precisely; the LED array interrupts ESS measurement; and there is inadequate optical contact between the ESS probe and the fiber optic plate (FOP) upon which the tissue sample is placed. The goal of this project is to further optimize the scanning module in order to remove malfunctions of the ESS software, provide a stable mechanical environment and increase the measurement speed, improve optical contact for quantitative ESS measurements, and build a protocol for assessing the deep margin of oral cancer tumors. The optimized module has been developed to measure quantitative spectral data that co-registers with a photograph of the scanned tissue. A device demo has successfully obtained the data from 10mm x 10mm boundary inked hotdog following the protocol developed in this thesis.

The transcription factor Runx1 has essential roles throughout hematopoiesis. Here, we demonstrate that Runx1 is critical for T cell maturation. Peripheral naïve CD4 + T cells from CD4-cre Runx1 cKO mice are phenotypically and functionally immature as shown by decreased production of TNF-α upon TCR stimulation. The loss of peripheral CD4 + T cells in CD4-cre Runx1 cKO mice is not due to defects in homeostasis or decreased expression of IL-7Rα, as transgenic expression of IL-7Rα does not rescue the loss of CD4 + T cells. Rather, immature Runx1-deficient CD4 + T cells are eliminated in the periphery by the activation and fixation of the classical complement pathway. In the thymus, there is a severe block in all aspects of intrathymic T cell maturation, although both positive and negative selection are unaltered. Thus, loss of Runx1 leads to the earliest characterized block in post-positive selection intrathymic maturation of CD4 T cells.

In the adult hippocampus, synapses are constantly formed and eliminated 1 , 2 . However, the exact function of synapse elimination in the adult brain, and how it is regulated, are largely unknown. Here we show that astrocytic phagocytosis 3 is important for maintaining proper hippocampal synaptic connectivity and plasticity. By using fluorescent phagocytosis reporters, we find that excitatory and inhibitory synapses are eliminated by glial phagocytosis in the CA1 region of the adult mouse hippocampus. Unexpectedly, we found that astrocytes have a major role in the neuronal activity-dependent elimination of excitatory synapses. Furthermore, mice in which astrocytes lack the phagocytic receptor MEGF10 show a reduction in the elimination of excitatory synapses; as a result, excessive but functionally impaired synapses accumulate. Finally, Megf10- knockout mice show defective long-term synaptic plasticity and impaired formation of hippocampal memories. Together, our data provide strong evidence that astrocytes eliminate unnecessary excitatory synaptic connections in the adult hippocampus through MEGF10, and that this astrocytic function is crucial for maintaining circuit connectivity and thereby supporting cognitive function. In adult mice, astrocytes carry out phagocytosis of excitatory hippocampal synapses through MEGF10 to maintain synaptic and circuit homeostasis.

Construction is among the leading industries/activities contributing the largest carbon footprint. This review paper aims to promote awareness of the sources of carbon footprint in the construction industry, from design to operation and management during manufacturing, transportation, construction, operations, maintenance and management, and end-of-life deconstruction phases. In addition, it summarizes the latest studies on carbon footprint reduction strategies in different phases of construction by the use of alternative additives in building materials, improvements in design, recycling construction waste, promoting the utility of alternative water resources, and increasing efficiencies of water technologies and other building systems. It was reported that the application of alternative additives/materials or techniques/systems can reduce up to 90% of CO2 emissions at different stages in the construction and building operations. Therefore, this review can be beneficial at the stage of conceptualization, design, and construction to assist clients and stakeholders in selecting materials and systems; consequently, it promotes consciousness of the environmental impacts of fabrication, transportation, and operation.

In the adult brain, neural circuit homeostasis depends on the constant turnover of synapses via astrocytic phagocytosis mechanisms. However, it remains unclear whether this process occurs in a circuit-specific manner. Here, we reveal that astrocytes target and eliminate specific type of excitatory synapses in the striatum. Using model mice lacking astrocytic phagocytosis receptors in the dorsal striatum, we found that astrocytes constantly remove corticostriatal synapses rather than thalamostriatal synapses. This preferential elimination suggests that astrocytes play a selective role in modulating corticostriatal plasticity and functions via phagocytosis mechanisms. Supporting this notion, corticostriatal long-term potentiation and the early phase of motor skill learning are dependent on astrocytic phagocytic receptors. Together, our findings demonstrate that astrocytes contribute to the connectivity and plasticity of the striatal circuit by preferentially engulfing a specific subset of excitatory synapses within brain regions innervated by multiple excitatory sources. Neural circuit homeostasis depends on astrocytic phagocytosis, but its circuit specificity remains unclear. Here, the authors show that astrocytes selectively eliminate corticostriatal synapses, regulating striatal plasticity and motor learning.