An Evaluation of International Students’ Perceptions About U.S. Institutions of Higher Education Post COVID-19

The problem addressed through this project is the decline in the retention of foreign students in U.S. institutions of higher learning due to the COVID-19 pandemic. In the 2020– 2021 school year, international student enrollment declined by 15%, demonstrating the direct impact of the pandemic on U.S. institutions of higher learning (Svrluga, 2021). Moreover, the financial contribution of foreign students dropped by 27% to $28.4 billion in the same financial year, which was attributed to perceptions among international students that they were unwelcome, in addition to visa processing challenges. The purpose of the study was to examine factors influencing the retention of foreign learners in U.S. higher education institutions during the COVID-19 pandemic. The study aimed to identify the unique challenges international students faced coping with the COVID-19 pandemic while in the United States. The study further examined some key interventions higher education institutions should have implemented to ensure international students’ experiences remained positive and existing challenges were resolved effectively. The study was guided by Spady’s model, Tinto\u27s theory, and the PICO framework (Considine et al., 2017; Nicoletti, 2019). The study was grounded on a systematic review of pertinent literature. The studies’ relevance to the research questions was derived from journals, conference proceedings, electronic databases of U.S. colleges and universities, research reports from research organizations, and other electronic databases such as JSTOR, ProQuest, ScienceDirect, and Emerald. The PRISMA 2009 flow diagram guided the process of selecting studies. Results from quantitative studies were compared based on the methodologies adopted and results found out. Qualitative studies that were included were analyzed thematically

MicroRNA miR-103a-3p targets NPAS3 to regulate progression of Alzheimer’s disease

Purpose: This study aimed at investigating miR-103a-3p expression, functional roles and underlying mechanism in regulating Alzheimer’s progression.Methods: RT-qPCR was used to assessed miR-103a-3p and NPAS3 expression in human neuroblastoma cells. Cell transfection of overexpressed or knocked down genes and CCK-8 assay measured cell viability while RT-qPCR was used to detect proliferation and apoptosis in biomarkers, Ki87 and PCNA, caspase-8 and caspase-3, respectively. Furthermore, luciferase assay was used to evaluate the luciferase activity while western blotting  analysis was applied to determine protein biomarkers regarding proliferation and apoptosis.Results: Expression of miR-103a-3p decreased but NPAS3 increased in AD cell lines. Overexpressed miR-103a-3p attenuated cell viability and NPAS3 bound miR-103a-3p to regulate AD progression. The inhibitory effect of miRNA on cell viability in AD was reversed by NPAS3.Conclusion: miR-103a-3p/NPAS3 might help to enrich knowledge on treatment of AD. Keywords: Alzheimer’s development, cell growth, cell proliferatio

Gadd45β and Gadd45γ are critical for regulating autoimmunity

The number of effector T cells is controlled by proliferation and programmed cell death. Loss of these controls on self-destructive effector T cells may precipitate autoimmunity. Here, we show that two members of the growth arrest and DNA damage-inducible (Gadd45) family, β and γ, are critical in the development of pathogenic effector T cells. CD4+ T cells lacking Gadd45β can rapidly expand and invade the central nervous system in response to myelin immunization, provoking an exacerbated and prolonged autoimmune encephalomyelitis in mice. Importantly, mice with compound deficiency in Gadd45β and Gadd45γ spontaneously developed signs of autoimmune lymphoproliferative syndrome and systemic lupus erythematosus. Our findings therefore identify the Gadd45β/Gadd45γ-mediated control of effector autoimmune lymphocytes as an attractive novel target for autoimmune disease therapy

Progress on Optical Fiber Biochemical Sensors Based on Graphene

Graphene, a novel form of the hexagonal honeycomb two-dimensional carbon-based structural material with a zero-band gap and ultra-high specific surface area, has unique optoelectronic capabilities, promising a suitable basis for its application in the field of optical fiber sensing. Graphene optical fiber sensing has also been a hotspot in cross-research in biology, materials, medicine, and micro-nano devices in recent years, owing to prospective benefits, such as high sensitivity, small size, and strong anti-electromagnetic interference capability and so on. Here, the progress of optical fiber biochemical sensors based on graphene is reviewed. The fabrication of graphene materials and the sensing mechanism of the graphene-based optical fiber sensor are described. The typical research works of graphene-based optical fiber biochemical sensor, such as long-period fiber grating, Bragg fiber grating, no-core fiber and photonic crystal fiber are introduced, respectively. Finally, prospects for graphene-based optical fiber biochemical sensing technology will also be covered, which will provide an important reference for the development of graphene-based optical fiber biochemical sensors

TRAF3 Negatively Regulates Platelet Activation and Thrombosis

CD40 ligand (CD40L), a member of the tumor necrosis factor (TNF) superfamily, binds to CD40, leading to many effects depending on target cell type. Platelets express CD40L and are a major source of soluble CD40L. CD40L has been shown to potentiate platelet activation and thrombus formation, involving both CD40-dependent and -independent mechanisms. A family of proteins called TNF receptor associated factors (TRAFs) plays key roles in mediating CD40L-CD40 signaling. Platelets express several TRAFs. It has been shown that TRAF2 plays a role in CD40L-mediated platelet activation. Here we show that platelet also express TRAF3, which plays a negative role in regulating platelet activation. Thrombin- or collagen-induced platelet aggregation and secretion are increased in TRAF3 knockout mice. The expression levels of collagen receptor GPVI and integrin αIIbβ3 in platelets were not affected by deletion of TRAF3, suggesting that increased platelet activation in the TRAF3 knockout mice was not due to increased expression platelet receptors. Time to formation of thrombi in a FeCl3-induced thrombosis model was significantly shortened in the TRAF3 knockout mice. However, mouse tail-bleeding times were not affected by deletion of TRAF3. Thus, TRAF3 plays a negative role in platelet activation and in thrombus formation in vivo

Critical success factors of collaborative approach in delivering sustainable construction

The essential aspect of sustainability in construction lead the complexities and involvement of multi parties in the construction project as well as its process. Conflicts of interests may appear in the process. Collaborative approach is essential for supporting decision making in delivering sustainable construction. This research identifies the collaboration critical factors. Scatter plot of mean and standard deviation analysis is done to rank the criticality of each collaboration factors in delivering sustainable construction. Eventually, factor analysis is done to identify the similarities between all the factors. There are twelve (12) factors identified from previous studies. Among all the collaboration factors, coordination among project stakeholders is identified as the most critical in delivering sustainable construction and followed by sharing responsibilities and mutual support. Based from factor analysis, five new factors of collaborative approach have been found

Volume-regulated Cl- current: contributions of distinct Cl- channel and localized Ca2+ signals.

The swelling-activated chloride current (ICl,swell) is induced when a cell swells and plays a central role in maintaining cell volume in response to osmotic stress. The major contributor of ICl,swell is the volume regulated anion channel (VRAC). LRRC8A (SWELL1) was recently identified as an essential component of VRAC but the mechanisms of VRAC activation are still largely unknown; moreover, other Cl- channels, such as anoctamin 1 (ANO1) were also suggested to contribute to ICl,swell. In this present study, we investigated the roles of LRRC8A and ANO1 in activation of ICl,swell; we also explored the role of intracellular Ca2+ in ICl,swell activation. We used CRISPR/Cas9 gene editing approach, electrophysiology, live fluorescent imaging, selective pharmacology and other approaches to show that both LRRC8A and ANO1 can be activated by cell swelling in HEK293 cells. Yet, both channels contribute biophysically and pharmacologically distinct components to ICl,swell, with LRRC8A being the major component. Cell swelling induced oscillatory Ca2+ transients and these Ca2+ signals were required to activate both, the LRRC8A- and ANO1-dependent components of ICl,swell. Both ICl,swell components required localized rather than global Ca2+ for activation. Interestingly, while intracellular Ca2+ was necessary and sufficient to activate ANO1, it was necessary but not sufficient to activate LRRC8A-mediated currents. Finally, Ca2+ transients linked to the ICl,swell activation were mediated by the GPCR-independent PLC isoforms

MYH9 is an Essential Factor for Porcine Reproductive and Respiratory Syndrome Virus Infection

Porcine reproductive and respiratory syndrome (PRRS) caused by the PRRS virus (PRRSV) is an important swine disease worldwide. PRRSV has a limited tropism for certain cells, which may at least in part be attributed to the expression of the necessary cellular molecules serving as the virus receptors or factors on host cells for virus binding or entry. However, these molecules conferring PRRSV infection have not been fully characterized. Here we show the identification of non-muscle myosin heavy chain 9 (MYH9) as an essential factor for PRRSV infection using the anti-idiotypic antibody specific to the PRRSV glycoprotein GP5. MYH9 physically interacts with the PRRSV GP5 protein via its C-terminal domain and confers susceptibility of cells to PRRSV infection. These findings indicate that MYH9 is an essential factor for PRRSV infection and provide new insights into PRRSV-host interactions and viral entry, potentially facilitating development of control strategies for this important swine disease