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This paper is organized into four sections followed by my personal recommendations: First, a brief section introduces the subject of Freedom Access to Information and freedom of expression, with relation to intellectual property, using a very broad brush, and sweeping strokes onto the human rights and governmental censorship. Second, some background useful baseline about the twenty & twenty first century’s development in information industry is presented as well as the affects of information industry on distance education, search engines, online access tools, online electronic databases, and knowledge management. Third, we have some baseline information on Egyptian current situation of IT and related activities. Fourth, the information technology infrastructure in Egypt, its development, components and roles is presented. Fifth, | present some personal recommendations. References.

The fabrication of complex and stable vasculature in engineered cardiac tissues represents a significant hurdle towards building physiologically relevant models of the heart. Here, we implemented a 3D model of cardiac vasculogenesis, incorporating endothelial cells (EC), stromal cells, and human induced pluripotent stem cell (iPSC)-derived cardiomyocytes (CM) in a fibrin hydrogel. The presence of CMs disrupted vessel formation in 3D tissues, resulting in the upregulation of endothelial activation markers and altered extracellular vesicle (EV) signaling in engineered tissues as determined by the proteomic analysis of culture supernatant. miRNA sequencing of CM- and EC-secreted EVs highlighted key EV-miRNAs that were postulated to play differing roles in cardiac vasculogenesis, including the let-7 family and miR-126-3p in EC-EVs. In the absence of CMs, the supplementation of CM-EVs to EC monolayers attenuated EC migration and proliferation and resulted in shorter and more discontinuous self-assembling vessels when applied to 3D vascular tissues. In contrast, supplementation of EC-EVs to the tissue culture media of 3D vascularized cardiac tissues mitigated some of the deleterious effects of CMs on vascular self-assembly, enhancing the average length and continuity of vessel tubes that formed in the presence of CMs. Direct transfection validated the effects of the key EC-EV miRNAs let-7b-5p and miR-126-3p in improving the maintenance of continuous vascular networks. EC-EV supplementation to biofabricated cardiac tissues and microfluidic devices resulted in tissue vascularization, illustrating the use of this approach in the engineering of enhanced, perfusable, microfluidic models of the myocardium., (Creative Commons Attribution license.)

The intricate anatomical structure and high cellular density of the myocardium complicate the bioengineering of perfusable vascular networks within cardiac tissues. In vivo neonatal studies highlight the key role of resident cardiac macrophages in post-injury regeneration and angiogenesis. Here, we integrate human pluripotent stem-cell-derived primitive yolk-sac-like macrophages within vascularized heart-on-chip platforms. Macrophage incorporation profoundly impacted the functionality and perfusability of microvascularized cardiac tissues up to 2 weeks of culture. Macrophages mitigated tissue cytotoxicity and the release of cell-free mitochondrial DNA (mtDNA), while upregulating the secretion of pro-angiogenic, matrix remodeling, and cardioprotective cytokines. Bulk RNA sequencing (RNA-seq) revealed an upregulation of cardiac maturation and angiogenesis genes. Further, single-nuclei RNA sequencing (snRNA-seq) and secretome data suggest that macrophages may prime stromal cells for vascular development by inducing insulin like growth factor binding protein 7 (IGFBP7) and hepatocyte growth factor (HGF) expression. Our results underscore the vital role of primitive macrophages in the long-term vascularization of cardiac tissues, offering insights for therapy and advancing heart-on-a-chip technologies., Competing Interests: Declaration of interests M.R. and Y.Z. are inventors on an issued patent that describes Biowire technology. This patent is licensed to Valo Health. M.R. and Y.Z. receive licensing revenue., (Copyright © 2024 Elsevier Inc. All rights reserved.)

Background: Obesity is a multifactorial metabolic disease resulting from behavioral and genetic factors. Obesity is linked to diabetes mellitus and hypertension, which are considered as major risk factors for chronic kidney disease (CKD); moreover, it has a direct effect on developing CKD and end stage renal disease (ESRD). Here was aimed to examine the association between uncoupling protein 2 (UCP2) gene expression and obesity in CKD patients., Methods: UCP2 gene expression was analyzed by real time polymerase chain reaction (RT-PCR) in 93 participants divided into three groups. The groups included 31 non-obese CKD patients, 31 obese CKD patients, and 31 healthy, age-matched, unrelated volunteers as a control group., Results: UCP2 gene expression was significantly relevant when comparing the non-obese CKD and obese CKD groups to the control group (p< 0.001). No significant association was found when the groups were compared by gender; Chi-square (X2) was 2.38 and p= 0.304. A significant negative correlation was found between UCP2 gene expression and BMI in CKD (p< 0.05)., Conclusion: These results indicate that UCP2 gene expression plays a significant role as a risk factor for obesity in CKD patients.

Endothelial progenitor cells (EPCs) promote the maintenance of the endothelium by secreting vasoreparative factors. A population of EPCs known as early outgrowth cells (EOCs) is being investigated as novel cell-based therapies for the treatment of cardiovascular disease. We previously demonstrated that the absence of liver X receptors (LXRs) is detrimental to the formation and function of EOCs under hypercholesterolemic conditions. Here, we investigate whether LXR activation in EOCs is beneficial for the treatment of atherosclerosis. EOCs were differentiated from the bone marrow of wild-type (WT) and LXR-knockout (Lxrαβ-/-) mice in the presence of vehicle or LXR agonist (GW3965). WT EOCs treated with GW3965 throughout differentiation showed reduced mRNA expression of endothelial lineage markers (Cd144, Vegfr2) compared with WT vehicle and Lxrαβ-/- EOCs. GW3965-treated EOCs produced secreted factors that reduced monocyte adhesion to activated endothelial cells in culture. When injected into atherosclerosis-prone Ldlr-/- mice, GW3965-treated EOCs, or their corresponding conditioned media (CM) were both able to reduce aortic sinus plaque burden compared with controls. Furthermore, when human EOCs (obtained from patients with established CAD) were treated with GW3965 and the CM applied to endothelial cells, monocyte adhesion was decreased, indicating that our results in mice could be translated to patients. Ex vivo LXR agonist treatment of EOCs therefore produces a secretome that decreases early atherosclerosis in Ldlr-/- mice, and additionally, CM from human EOCs significantly inhibits monocyte to endothelial adhesion. Thus, active factor(s) within the GW3965-treated EOC secretome may have the potential to be useful for the treatment of atherosclerosis., (© 2020 The Authors. STEM CELLS TRANSLATIONAL MEDICINE published by Wiley Periodicals LLC on behalf of AlphaMed Press.)

Placental extravillous trophoblast (EVT) invasion is essential in establishing proper blood supply to the fetus during pregnancy. However, traditional 2D in vitro systems do not model the in vivo invasion process in an anatomically-relevant manner. Our objectives were to develop a 3D spheroid model that would allow better emulation of placental invasion in vitro and to characterize the transcriptomic and functional outcomes. HTR8/SVneo EVT cells were self-assembled into 3D spheroids using ultra-low attachment plates. Transcriptomic profiling followed by gene set enrichment and gene ontology analyses revealed major global transcriptomic differences, with significant up-regulations in EVTs cultured as 3D spheroids in canonical pathways and biological processes such as immune response, angiogenesis, response to stimulus, wound healing, and others. These findings were further validated by RT-qPCR, showing significant up-regulations in genes and/or proteins related to epithelial-mesenchymal transition, cell-cell contact, angiogenesis, and invasion/migration. A high-throughput, spheroid invasion assay was applied to reveal the dynamic invasion of EVTs away from the spheroid core into extracellular matrix. Lastly, lipopolysaccharide, dexamethasone, or Δ 9 -tetrahydrocannabinol exposure was found to impact the invasion of EVT spheroids. Altogether, we present a well-characterized, 3D spheroid model of EVT invasion and demonstrate its potential use in drug and toxin screening during pregnancy.

Diffuse Large B-cell lymphoma (DLBCL) is an aggressive disease with heterogeneous outcome and marked variable response to chemotherapy. We assessed promoter hypermethylation (PM) for a panel of tumor suppressor genes in 75 DLBCLs compared to 20 lymphoid hyperplasia (LH) and 30 normal control, using methylation specific PCR. Results were correlated to patients' clinic-pathological characteristics, immunophenotyping, and patients' outcome. DAPK1, RUNX3, MT1G, MGMT, CDH1 and p16 PM were detected in 38.7% (29/75), 49.3% (37/75), 46.7% (35/75), 44% (33/75), 49.3% (37/75) and 42.7% (32/75);respectively, of DLBCL patients compared to LH group (P < 0.05). Aberrant PM of RUNX3, MGMT, CDH1 and p16 was significantly higher in non-germinal central B-cell like (non-GCB) compared to GCB (58.3% vs. 33.3%, 56.2% vs. 22.2, 62.5% vs. 25.9, and 56.2% vs. 18.5%, respectively). PM of studies genes in DLBCL associated significantly with worse survival outcome and resistance to chemotherapy (P ≤ 0.01). In non-GCB group, DAPK1, MT1G, RUNX3, CDH1 and p16 PM associated significantly with reduced DFS (P ≤ 0.004) and OS (P ≤ 0.015). Multivariate analysis indicated that RUNX3 and CDH1 PM were independent prognostic factors for OS (P = 0.03 and 0.04; respectively), while DAPK1, RUNX3 and MT1G PM were independent prognostic factors for DFS (P = 0.002, 0.037& 0.007; respectively). DAPK1, RUNX3, MT1G, CDH1 and p16 PM are promising prognostic and/or predictive markers for non-GCB independent of IPI. Upregulation of those genes using new demethylating agents is a promising approach that sensitize chemoresistant DLBCL patients, especially the non-GCB subtype.

The incorporation of the extracellular matrix (ECM) is essential for generating in vitro models that truly represent the microarchitecture found in human tissues. However, the cell-cell and cell-ECM interactions in vitro remains poorly understood in placental trophoblast biology. We investigated the effects of varying the surface properties (surface thickness and stiffness) of two ECMs, collagen I and Matrigel, on placental trophoblast cell morphology, viability, proliferation, and expression of markers involved in differentiation/syncytial fusion. Most notably, thicker Matrigel surfaces were found to induce the self-assembly of trophoblast cells into 3D spheroids that exhibited thickness-dependent changes in viability, proliferation, syncytial fusion, and gene expression profiles compared to two-dimensional cultures. Changes in F-actin organization, cell spread morphologies, and integrin and matrix metalloproteinase gene expression profiles, further reveal that the response to surface thickness may be mediated in part through cellular stiffness-sensing mechanisms. Our derivation of self-assembling trophoblast spheroid cultures through regulation of ECM surface alone contributes to a deeper understanding of cell-ECM interactions, and may be important for the advancement of in vitro platforms for research or diagnostics., Competing Interests: Dr. Tom Ewart, a member of our research team, is employed by Evik Diagnostics, Ottawa Canada. Dr. Ewart provides in-kind consultancy for this expertise in surface chemistry and its connection to 3 dimensional cell culture growth. His involvement in this project is purely academic and this commercial affiliation does not alter our adherence to all PLOS ONE policies on sharing data and materials.

Immunogenicity of inactivated tissue-culture-derived duck enteritis virus (DEV) vaccines was evaluated in white Pekin and mallard ducks. DEV from a Lake Andes outbreak was propagated in chicken embryo fibroblast cells, inactivated with beta-propiolactone, and emulsified with Freund's adjuvant (FA), multiple-oil emulsion (MOE), or Squalane-pluronic L121 (L121). White Pekin and mallard ducklings were vaccinated at 2 or 3 wk of age, respectively. Challenge at 2 wk postvaccination with a virulent DEV isolated from a Long Island outbreak indicated that inactivated Lake Andes (ILA) vaccine mixed with any of the above adjuvants conferred protection, even with a single-dose inoculation. Antibody responses to vaccination, as determined by indirect enzyme-linked immunosorbent assay, showed that ILA virus with FA induced an early production of antibodies similar to that induced by commercially available modified live virus (MLV) vaccine. However, the mean anti-duck virus enteritis (DVE) IgG titers determined by multiple samplings during the first 35 days postvaccination showed titers from ILA virus with FA to be at least 10 times higher than those induced by MLV vaccine. The highest antibody titers were induced by ILA mixed with FA followed by ILA mixed with the MOE and L121. The results of this study indicated that inactivated vaccine is as efficacious as modified live vaccine in enhancing protection against virulent DEV in waterfowl.

Turkey poults from hens vaccinated against avian group A rotavirus were examined to study the transfer of maternally derived anti-rotavirus IgG (rIgG) to the mucosal surfaces (intestinal and tracheal), serum, yolk, and bile. During the first week of life, maternal rIgG titers in intestinal mucosal washings were 200-to-500-fold less than rIgG titers in the circulation, as determined by enzyme-linked immunosorbent assay (ELISA). The intestinal titers in 10- and 13-day-old poults were negligible. A moderate linear correlation (r = 0.6) was present between rIgG titer in the blood circulation and the intestines, with a serum cutoff level of 10,000 ELISA units. Maternal rIgG was detected in tracheal washings only during the first 3 days of life. Biliary rIgG titers were fourfold higher than intestinal titers at day of hatch but had declined considerably in 1-day-old poults. Yolk had relatively high rIgG titers at hatching. Maternal rIgG titer in the small intestine was determined after in situ ligation of the individual segments; it was highest in the duodenum, followed by the ileum and jejunum. There was evidence that rIgG in the intestine was transferred from the blood and not directly from the yolk sac. Bidirectional movement of rIgG between circulation and intestine was also detected. Maternal rIgG was not detected in the intestinal washings of progeny from hens naturally infected with rotavirus.

The effect of circulating maternally transferred IgG on immunity of turkey poults to rotavirus infections was investigated. Specific-pathogen-free (SPF) turkey hens were hyperimmunized with avian group A rotavirus 2 weeks before the laying cycle. SPF poults designated positive for group A rotavirus (Rab+) and negative for such maternal antibody (Rab-) were challenged orally with the homologous virus at 2, 5, or 12 days of age (challenge Groups 1, 2, and 3, respectively). Poults were examined at 3 and 6 days postinfection (PI) for clinical signs, gross lesions, histopathological changes in the small intestine, rotavirus in intestinal contents, and D-xylose absorption as an indicator of the intestinal absorptive function. In challenge Groups 1 and 2, rotavirus titers in the intestinal contents were significantly lower in Rab+ poults than in Rab- poults at 3 days PI. Gross lesions and D-xylose absorption results were consistent with the virus-shedding data. Histopathological changes were moderate and comparable in Rab- and Rab+ poults. In challenge Group 3, however, no significant differences were observed between Rab- and Rab+ poults in any of the examined parameters. Results provided evidence that circulating maternally derived IgG has an important role in protection of the intestinal mucosa against rotavirus infection during the first week of life. It is suggested that protective immunity afforded by maternal IgG is titer-dependent.