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The novel coronavirus (COVID-19) pandemic has altered every aspect of life across the world. The global economy, health care systems, social life and most importantly education have all been affected. The severity of the virus forced students, educators, and all other non-essential workers to confine to their respective homes to limit the spread of the virus. Many states have enacted curfew laws, restaurants and grocery stores have established new rules and regulations, and teachers are obliged to alter their teaching pedagogy from the face physical walls of the classroom [face-to-face learning] to web-based distance learning. The resulted massive exposure towards web-based learning is well administered by institutions with previous competency while other institutions find it difficult to operate remotely. This communication briefly examines the nature of web-based learning caused by the COVID-19 global pandemic.

As graduate assistants (GAs) at the Graduate Center for the Study of Early Learning at the University of Mississippi, two of the authors participated in a trip to Money, Mississippi, the community where one of the most horrific events related to racial unrest in the country's history occurred. While there, they learned about Emmett Till, a young black teen who sparked the civil rights movement. They got to see where Emmett was accused of flirting with a white woman back in 1955, the location of where he was accused, and a museum, Sumner Courthouse Museum that was created in remembrance of him which was also reported as the place his body was left after his murder. Emmett Till is a major part of Mississippi history and the civil rights movement; sadly however, Emmett's story is not taught in some schools. This article constitutes a reflection of "new to the field" early childhood educators on how place-based experiences influence how and what is taught. The two GAs present their own stories in their own voice and combine thoughts with their guide in a concluding section, which challenges all seasoned educators to reflect on their own teaching.

Abstract This study investigates the development of thermoplastic polyurethane (TPU) filaments incorporating multi‐walled carbon nanotubes (MWCNT) to enhance strain‐sensing capabilities. Various MWCNT reinforcement ratios are used to produce customized feedstock for fused filament fabrication (FFF) 3D printing. Mechanical properties and the piezoresistive response of samples printed with these multifunctional filaments are concurrently evaluated. Surface morphology and microstructural observations reveal that higher MWCNT weight percentages increase filament surface roughness and rigidity. The microstructural modifications directly influence the tensile strength and strain energy of the printed samples. The study identifies an apparent percolation threshold within the 10–12 wt.% MWCNT range, indicating the formation of a conductive network. At this threshold, higher gauge factors are achieved at lower strains. A newly introduced Electro‐Mechanical Sensitivity Ratio (ESR) parameter enables the classification of composite behaviors into two distinct zones, offering the ability to tailor self‐sensing structures with on‐demand properties. Finally, flexible structures with proven application in soft robotics and shape morphing are fabricated and tested at different loading conditions to demonstrate the potential applicability of the custom filaments produced. The results highlight a pronounced piezoresistive response and superior load‐bearing performance in the examined structures.

Lactococcus garviae (L. garviae) is a gram-positive coccus belonging to the Streptococcaceae family. While primarily a pathogen in fish farms causing hemorrhagic sepsis, it can act as a rare opportunistic pathogen in humans. A 2021 case report by Bravo et al. documented less than 30 cases of infective endocarditis caused by L. garviae worldwide at that time [1]. This case report describes the 27th documented case globally and 7th documented case in the USA of L. garviae causing infective endocarditis of a prosthetic valve [1].L. garviae is found in unpasteurized dairy products, raw fish, and meat (pork, beef, and poultry), but the route of human transmission remains unclear [3]. It seems to have a predilection for individuals with prosthetic valves, immunocompromised states, prior gastrointestinal surgery, gastrointestinal disorders (colon polyps and diverticulosis), and the use of acid-reducing medications [1-3]. Infective endocarditis is the most common systemic disease caused by L. garviae [1-4].This report details the case of a 75-year-old male, with multiple comorbidities and risk factors for L. garviae infection who was admitted for “symptomatic anemia”. High clinical suspicion, coupled with an inadequate hemoglobin response to transfusion, a normal anemia workup, and blood cultures positive for L. garviae, promoted a transesophageal echocardiogram (TEE). However, the results were negative. Consequently, an 18F-fluorodeoxyglucose positron emission tomography/computed tomography scan (18FDG PET/CT) was performed. The scan revealed increased uptake in the aortic valve replacement consistent with prosthetic valve endocarditis in the setting of Lactococcus garviae bacteremia.

Advanced age is associated with an increased susceptibility to Coronavirus Disease (COVID)-19 and more severe outcomes, although the underlying mechanisms are understudied. The lung endothelium is located next to infected epithelial cells and bystander inflammation may contribute to thromboinflammation and COVID-19-associated coagulopathy. Here, we investigated age-associated SARS-CoV-2 pathogenesis and endothelial inflammatory responses using humanized K18-hACE2 mice. Survival was reduced to 20% in aged mice (85–112 weeks) versus 50% in young mice (12–15 weeks) at 10 days post infection (dpi). Bulk RNA-sequencing of endothelial cells from mock and infected mice at 2dpi of both age groups (aged: 72–85 weeks; young: 15 weeks) showed substantially lower significant differentially regulated genes in infected aged mice than in young mice (712 versus 2294 genes). Viral recognition and anti-viral pathways such as RIG-I-like receptor signaling, NOD-like receptor signaling and interferon signaling were regulated in response to SARS-CoV-2. Young mice showed several fold higher interferon responses (Ifitm3, Ifit1, Isg15, Stat1) and interferon-induced chemokines (Cxcl10 and Cxcl11) than aged mice. Endothelial cells from infected young mice displayed elevated expression of chemokines (Cxcl9, Ccl2) and leukocyte adhesion markers (Icam1) underscoring that inflammation of lung endothelium during infection could facilitate leukocyte adhesion and thromboinflammation. TREM1 and acute phase response signaling were particularly prominent in endothelial cells from infected young mice. Immunohistochemistry was unable to detect viral protein in pulmonary endothelium. In conclusion, our data demonstrate that the early host response of the endothelium to SARS-CoV-2 infection declines with aging, which could be a potential contributor to disease severity.

Hepatitis E virus (HEV) is the leading cause of acute viral hepatitis worldwide. HEV associated pregnancy mortality has been reported as up to 30% in humans. Recent findings suggest HEV may elicit effects directly in the reproductive system with HEV protein found in the testis, viral RNA in semen, and viral replication occurring in placental cell types. Using a natural host model for HEV infection, pigs, we demonstrate infectious HEV within the mature spermatozoa and altered sperm viability from HEV infected pigs. HEV isolated from sperm remained infectious suggesting a potential transmission route via sexual partners. Our findings suggest that HEV should be explored as a possible sexually transmittable disease. Our findings propose that infection routes outside of oral and intravenous infection need to be considered for their potential to contribute to higher mortality in HEV infections when pregnancy is involved and in HEV disease in general.

ABSTRACT: The poultry industry is evolving towards antibiotic-free production to meet market demands and decelerate the increasing spread of the antimicrobial resistance. The growing need for antibiotic free products has challenged producers to decrease or completely stop using antimicrobials as feed supplements in broiler diet to improve feed efficiency, growth rate, and intestinal health. Natural feed additives (e.g., probiotics and phytobiotics) are promising alternatives to substitute antimicrobial growth promoters. The goal of our study was to characterize the effects of a Probiotic and an Essential Oils blend on broilers’ performance and perform a time-series analysis to describe their excreta microbiome. A total of 320 Cobb 500 (1-day-old) chicks were raised for 21 d in 32 randomly allocated cages. Treatments consisted of 4 experimental diets: a basal diet, and a basal diet mixed with an Antibiotic (bacitracin methylene disalicylate), an essential oils blend (oregano oil, rosemary, and red pepper), or a Probiotic (Bacillus subtilis). Body weight (on 1, 10, and 21d), and feed intake (10d and 21d) were recorded and feed conversion ratio was calculated. Droppings were collected daily (1–21d) to characterize broilers’ excreta microbiota by targeted sequencing of the bacterial 16S rRNA gene. The Probiotic significantly improved feed conversion ratio for starter phase 1 to 10d (P = 0.03), grower phase 10 to 21d (P = 0.05), and total period 1 to 21d (P = 0.01) compared to the Antibiotic. Feed supplements did not affect alpha diversity but did impact microbial beta diversity (P < 0.01). Age also impacted microbiome turnover as differences in alpha and beta diversity were detected. Furthermore, when compared to the basal diet, the probiotic and antibiotic significantly impacted relative abundance of Bifidobacterium (log2 fold change −1.44, P = 0.03), Intestinimonas (log2 fold change 0.560, P < 0.01) and Ligilactobacillus (log2 fold change −1.600, P < 0.01). Overall, Probiotic supplementation but not essential oils supplementation positively impacted broilers’ growth performance by directly causing directional shifts in broilers’ excreta microbiota structure.

Epstein-Barr virus (EBV) is an important cause of human lymphomas, including Burkitt lymphoma (BL). EBV+ BLs are driven by Myc translocation and have stringent forms of viral latency that do not express either of the two major EBV oncoproteins, EBNA2 (which mimics Notch signaling) and LMP1 (which activates NF-κB signaling). Suppression of Myc-induced apoptosis, often through mutation of the TP53 (p53) gene or inhibition of pro-apoptotic BCL2L11 (BIM) gene expression, is required for development of Myc-driven BLs. EBV+ BLs contain fewer cellular mutations in apoptotic pathways compared to EBV-negative BLs, suggesting that latent EBV infection inhibits Myc-induced apoptosis. Here we use an EBNA2-deleted EBV virus (ΔEBNA2 EBV) to create the first in vivo model for EBV+ BL-like lymphomas derived from primary human B cells. We show that cord blood B cells infected with both ΔEBNA2 EBV and a Myc-expressing vector proliferate indefinitely on a CD40L/IL21 expressing feeder layer in vitro and cause rapid onset EBV+ BL-like tumors in NSG mice. These LMP1/EBNA2-negative Myc-driven lymphomas have wild type p53 and very low BIM, and express numerous germinal center B cell proteins (including TCF3, BACH2, Myb, CD10, CCDN3, and GCSAM) in the absence of BCL6 expression. Myc-induced activation of Myb mediates expression of many of these BL-associated proteins. We demonstrate that Myc blocks LMP1 expression both by inhibiting expression of cellular factors (STAT3 and Src) that activate LMP1 transcription and by increasing expression of proteins (DNMT3B and UHRF1) known to enhance DNA methylation of the LMP1 promoters in human BLs. These results show that latent EBV infection collaborates with Myc over-expression to induce BL-like human B-cell lymphomas in mice. As NF-κB signaling retards the growth of EBV-negative BLs, Myc-mediated repression of LMP1 may be essential for latent EBV infection and Myc translocation to collaboratively induce human BLs.

Mitochondrial dysfunction is associated with several retinal degenerative diseases including Age-related Macular Degeneration (AMD). Human mitochondrial DNA (mtDNA) haplogroups are inherited from a common ancestral clan and are defined by specific sets of genetic differences. The purpose of this study was to determine and compare the effects of mtDNA haplogroups H and J on transcriptome regulation and cellular resilience to oxidative stress in human RPE cytoplasmic hybrid (cybrid) cell lines in vitro. ARPE-19 cybrid cell lines containing mtDNA haplogroups H and J were created by fusing platelets obtained from normal individuals containing H and J haplogroups with mitochondria-deficient (Rho0) ARPE-19 cell lines. These cybrids were exposed to oxidative stress using 300 μM hydrogen peroxide (H2O2), following which mitochondrial structural dynamics was studied at varying time points using the mitochondrial markers - TOMM20 (Translocase of Outer Mitochondrial Membrane 20) and Mitotracker. To evaluate mitochondrial function, levels of ROS, ΔΨm and [Ca2+]m were measured using flow cytometry, and ATP levels were measured using luminescence. The H and J cybrid cell transcriptomes were compared using RNAseq to determine how changes in mtDNA regulate gene expression. Inflammatory and angiogenic markers were measured using Luminex assay to understand how these mtDNAs influenced cellular response to oxidative stress. Actin filaments' morphology was examined using confocal microscopy. Following exposure to H2O2 stress, the J cybrids showed increased mitochondrial swelling and perinuclear localization, disturbed fission and fusion, increased calcium uptake (p