Journal articles: 'Cell transmission models'

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Ahmed, Afzal, Mir Shabbar Ali, and Toor Ansari. "Modelling Heterogeneous and Undisciplined Traffic Flow using Cell Transmission Model." International Journal of Traffic and Transportation Management 02, no. 01 (November 11, 2020): 01–05. http://dx.doi.org/10.5383/jttm.02.01.001.

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This research calibrates Cell Transmission Model (CTM) for heterogeneous and non-lane disciplined traffic, as observed in Pakistan and some other developing countries by constructing a flow-density fundamental traffic flow diagram. Currently, most of the traffic simulation packages used for such heterogonous and non-lane-disciplined traffic are not calibrated for local traffic conditions and most of the traffic flow models are developed for comparatively less heterogeneous and lane-disciplined traffic. The flow-density fundamental traffic flow diagram is developed based on extensive field data collected from Karachi, Pakistan. The calibrated CTM model is validated by using actual data from another road and it was concluded that CTM is capable of modelling heterogeneous and non-lane disciplined traffic and performed very reasonably. The calibrated CTM will be a useful input for the application of traffic simulation and optimization packages such as TRANSYT, SIGMIX, DISCO, and CTMSIM.

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Pourbashash, Hossein, Sergei S. Pilyugin, Patrick De Leenheer, and Connell McCluskey. "Global analysis of within host virus models with cell-to-cell viral transmission." Discrete & Continuous Dynamical Systems - B 19, no. 10 (2014): 3341–57. http://dx.doi.org/10.3934/dcdsb.2014.19.3341.

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Fu, Rebecca Menhua, Charlotte Caroline Decker, and Viet Loan Dao Thi. "Cell Culture Models for Hepatitis E Virus." Viruses 11, no. 7 (July 3, 2019): 608. http://dx.doi.org/10.3390/v11070608.

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Despite a growing awareness, hepatitis E virus (HEV) remains understudied and investigations have been historically hampered by the absence of efficient cell culture systems. As a result, the pathogenesis of HEV infection and basic steps of the HEV life cycle are poorly understood. Major efforts have recently been made through the development of HEV infectious clones and cellular systems that significantly advanced HEV research. Here, we summarize these systems, discussing their advantages and disadvantages for HEV studies. We further capitalize on the need for HEV-permissive polarized cell models to better recapitulate the entire HEV life cycle and transmission.

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Kumberger, Peter, Karina Durso-Cain, Susan Uprichard, Harel Dahari, and Frederik Graw. "Accounting for Space—Quantification of Cell-To-Cell Transmission Kinetics Using Virus Dynamics Models." Viruses 10, no. 4 (April 17, 2018): 200. http://dx.doi.org/10.3390/v10040200.

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Allen, Linda J. S., and Elissa J. Schwartz. "Free-virus and cell-to-cell transmission in models of equine infectious anemia virus infection." Mathematical Biosciences 270 (December 2015): 237–48. http://dx.doi.org/10.1016/j.mbs.2015.04.001.

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Alimardani, Fatemeh, and John S. Baras. "Performance Assessment of Different Cell-Transmission Models for Ramp-Metered Highway Networks." IFAC-PapersOnLine 54, no. 2 (2021): 114–20. http://dx.doi.org/10.1016/j.ifacol.2021.06.016.

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Recasens, Ariadna, Ayse Ulusoy, Philipp J. Kahle, Donato A. Di Monte, and Benjamin Dehay. "In vivo models of alpha-synuclein transmission and propagation." Cell and Tissue Research 373, no. 1 (November 29, 2017): 183–93. http://dx.doi.org/10.1007/s00441-017-2730-9.

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Graw, Frederik, Danyelle N. Martin, Alan S. Perelson, Susan L. Uprichard, and Harel Dahari. "Quantification of Hepatitis C Virus Cell-to-Cell Spread Using a Stochastic Modeling Approach." Journal of Virology 89, no. 13 (April 1, 2015): 6551–61. http://dx.doi.org/10.1128/jvi.00016-15.

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ABSTRACTIt has been proposed that viral cell-to-cell transmission plays a role in establishing and maintaining chronic infections. Thus, understanding the mechanisms and kinetics of cell-to-cell spread is fundamental to elucidating the dynamics of infection and may provide insight into factors that determine chronicity. Because hepatitis C virus (HCV) spreads from cell to cell and has a chronicity rate of up to 80% in exposed individuals, we examined the dynamics of HCV cell-to-cell spreadin vitroand quantified the effect of inhibiting individual host factors. Using a multidisciplinary approach, we performed HCV spread assays and assessed the appropriateness of different stochastic models for describing HCV focus expansion. To evaluate the effect of blocking specific host cell factors on HCV cell-to-cell transmission, assays were performed in the presence of blocking antibodies and/or small-molecule inhibitors targeting different cellular HCV entry factors. In all experiments, HCV-positive cells were identified by immunohistochemical staining and the number of HCV-positive cells per focus was assessed to determine focus size. We found that HCV focus expansion can best be explained by mathematical models assuming focus size-dependent growth. Consistent with previous reports suggesting that some factors impact HCV cell-to-cell spread to different extents, modeling results estimate a hierarchy of efficacies for blocking HCV cell-to-cell spread when targeting different host factors (e.g., CLDN1 > NPC1L1 > TfR1). This approach can be adapted to describe focus expansion dynamics under a variety of experimental conditions as a means to quantify cell-to-cell transmission and assess the impact of cellular factors, viral factors, and antivirals.IMPORTANCEThe ability of viruses to efficiently spread by direct cell-to-cell transmission is thought to play an important role in the establishment and maintenance of viral persistence. As such, elucidating the dynamics of cell-to-cell spread and quantifying the effect of blocking the factors involved has important implications for the design of potent antiviral strategies and controlling viral escape. Mathematical modeling has been widely used to understand HCV infection dynamics and treatment response; however, these models typically assume only cell-free virus infection mechanisms. Here, we used stochastic models describing focus expansion as a means to understand and quantify the dynamics of HCV cell-to-cell spreadin vitroand determined the degree to which cell-to-cell spread is reduced when individual HCV entry factors are blocked. The results demonstrate the ability of this approach to recapitulate and quantify cell-to-cell transmission, as well as the impact of specific factors and potential antivirals.

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Wang, Shaoli, Achun Zhang, and Fei Xu. "Dynamical analysis for delayed virus infection models with cell-to-cell transmission and density-dependent diffusion." International Journal of Biomathematics 13, no. 07 (August 20, 2020): 2050060. http://dx.doi.org/10.1142/s1793524520500606.

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In this paper, certain delayed virus dynamical models with cell-to-cell infection and density-dependent diffusion are investigated. For the viral model with a single strain, we have proved the well-posedness and studied the global stabilities of equilibria by defining the basic reproductive number [Formula: see text] and structuring proper Lyapunov functional. Moreover, we found that the infection-free equilibrium is globally asymptotically stable if [Formula: see text], and the infection equilibrium is globally asymptotically stable if [Formula: see text]. For the multi-strain model, we found that all viral strains coexist if the corresponding basic reproductive number [Formula: see text], while virus will extinct if [Formula: see text]. As a result, we found that delay and the density-dependent diffusion does not influence the global stability of the model with cell-to-cell infection and homogeneous Neumann boundary conditions.

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박민주, 권오훈, and Byung-doo JUNG. "Effect Analysis of Bus-exclusive Lane on Traffic Congestion Using Cell Transmission Models." Journal of Transport Research 22, no. 3 (September 2015): 43–53. http://dx.doi.org/10.34143/jtr.2015.22.3.43.

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Jansen, J. A., E. T. Den Braber, X. F. Walboomers, and J. E. De Ruijter. "Soft Tissue and Epithelial Models." Advances in Dental Research 13, no. 1 (June 1999): 57–66. http://dx.doi.org/10.1177/08959374990130011601.

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The applicability of a biomaterial for the manufacturing of oral implants is determined by its physicochemical and geometric surface properties. Research, therefore, is concerned with the cellular reactions that occur when an implant material comes into contact with body tissues. For permucosal oral implants, this involves both the reaction of bone and gingival cells. In vitro cell culturing-including the use of various analytical techniques like light microscopy, scanning and transmission electron microscopy, confocal laser scanning microscopy, and digital image analysis-is a good tool whereby investigators can obtain more insight into the relevant components of implant-tissue adhesion. In the current overview, the role of cell models in oral implant research is discussed, specifically with reference to responses of epithelial cells and fibroblasts.

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Harischandra, Dilshan S., Dharmin Rokad, Matthew L. Neal, Shivani Ghaisas, Sireesha Manne, Souvarish Sarkar, Nikhil Panicker, et al. "Manganese promotes the aggregation and prion-like cell-to-cell exosomal transmission of α-synuclein." Science Signaling 12, no. 572 (March 12, 2019): eaau4543. http://dx.doi.org/10.1126/scisignal.aau4543.

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The aggregation of α-synuclein (αSyn) is considered a key pathophysiological feature of certain neurodegenerative disorders, collectively termed synucleinopathies. Given that a prion-like, cell-to-cell transfer of misfolded αSyn has been recognized in the spreading of αSyn pathology in synucleinopathies, we investigated the biological mechanisms underlying the propagation of the disease with respect to environmental neurotoxic stress. Considering the potential role of the divalent metal manganese (Mn2+) in protein aggregation, we characterized its effect on αSyn misfolding and transmission in experimental models of Parkinson’s disease. In cultured dopaminergic neuronal cells stably expressing wild-type human αSyn, misfolded αSyn was secreted through exosomes into the extracellular medium upon Mn2+ exposure. These exosomes were endocytosed through caveolae into primary microglial cells, thereby mounting neuroinflammatory responses. Furthermore, Mn2+-elicited exosomes exerted a neurotoxic effect in a human dopaminergic neuronal model (LUHMES cells). Moreover, bimolecular fluorescence complementation (BiFC) analysis revealed that Mn2+ accelerated the cell-to-cell transmission of αSyn, resulting in dopaminergic neurotoxicity in a mouse model of Mn2+ exposure. Welders exposed to Mn2+ had increased misfolded αSyn content in their serum exosomes. Stereotaxically delivering αSyn-containing exosomes, isolated from Mn2+-treated αSyn-expressing cells, into the striatum initiated Parkinsonian-like pathological features in mice. Together, these results indicate that Mn2+ exposure promotes αSyn secretion in exosomal vesicles, which subsequently evokes proinflammatory and neurodegenerative responses in both cell culture and animal models.

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Forlani, Greta, Mariam Shallak, Roberto Sergio Accolla, and Maria Grazia Romanelli. "HTLV-1 Infection and Pathogenesis: New Insights from Cellular and Animal Models." International Journal of Molecular Sciences 22, no. 15 (July 27, 2021): 8001. http://dx.doi.org/10.3390/ijms22158001.

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Since the discovery of the human T-cell leukemia virus-1 (HTLV-1), cellular and animal models have provided invaluable contributions in the knowledge of viral infection, transmission and progression of HTLV-associated diseases. HTLV-1 is the causative agent of the aggressive adult T-cell leukemia/lymphoma and inflammatory diseases such as the HTLV-1 associated myelopathy/tropical spastic paraparesis (HAM/TSP). Cell models contribute to defining the role of HTLV proteins, as well as the mechanisms of cell-to-cell transmission of the virus. Otherwise, selected and engineered animal models are currently applied to recapitulate in vivo the HTLV-1 associated pathogenesis and to verify the effectiveness of viral therapy and host immune response. Here we review the current cell models for studying virus–host interaction, cellular restriction factors and cell pathway deregulation mediated by HTLV products. We recapitulate the most effective animal models applied to investigate the pathogenesis of HTLV-1-associated diseases such as transgenic and humanized mice, rabbit and monkey models. Finally, we summarize the studies on STLV and BLV, two closely related HTLV-1 viruses in animals. The most recent anticancer and HAM/TSP therapies are also discussed in view of the most reliable experimental models that may accelerate the translation from the experimental findings to effective therapies in infected patients.

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Bignon, Yohan, Virginie Poindessous, Luca Rampoldi, Violette Haldys, and Nicolas Pallet. "Chemically based transmissible ER stress protocols are unsuitable to study cell-to-cell UPR transmission." Biochemical Journal 477, no. 20 (October 29, 2020): 4037–51. http://dx.doi.org/10.1042/bcj20200699.

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Renal epithelial cells regulate the destructive activity of macrophages and participate in the progression of kidney diseases. Critically, the Unfolded Protein Response (UPR), which is activated in renal epithelial cells in the course of kidney injury, is required for the optimal differentiation and activation of macrophages. Given that macrophages are key regulators of renal inflammation and fibrosis, we suppose that the identification of mediators that are released by renal epithelial cells under Endoplasmic Reticulum (ER) stress and transmitted to macrophages is a critical issue to address. Signals leading to a paracrine transmission of ER stress (TERS) from a donor cell to a recipient cells could be of paramount importance to understand how ER-stressed cells shape the immune microenvironment. Critically, the vast majority of studies that have examined TERS used thaspigargin as an inducer of ER stress in donor cells in cellular models. By using multiple sources of ER stress, we evaluated if human renal epithelial cells undergoing ER stress can transmit the UPR to human monocyte-derived macrophages and if such TERS can modulate the inflammatory profiles of these cells. Our results indicate that carry-over of thapsigargin is a confounding factor in chemically based TERS protocols classically used to induce ER Stress in donor cells. Hence, such protocols are not suitable to study the TERS phenomenon and to identify its mediators. In addition, the absence of TERS transmission in more physiological models of ER stress indicates that cell-to-cell UPR transmission is not a universal feature in cultured cells.

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Ali, Md Shipon, Ekram Hossain, and Dong In Kim. "Coordinated Multipoint Transmission in Downlink Multi-Cell NOMA Systems: Models and Spectral Efficiency Performance." IEEE Wireless Communications 25, no. 2 (April 2018): 24–31. http://dx.doi.org/10.1109/mwc.2018.1700094.

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Doan, Kien, and Satish V. Ukkusuri. "On the holding-back problem in the cell transmission based dynamic traffic assignment models." Transportation Research Part B: Methodological 46, no. 9 (November 2012): 1218–38. http://dx.doi.org/10.1016/j.trb.2012.05.001.

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Moench, T. R. "Cell-Associated Transmission of HIV Type 1 and Other Lentiviruses in Small-Animal Models." Journal of Infectious Diseases 210, suppl 3 (November 20, 2014): S654—S659. http://dx.doi.org/10.1093/infdis/jiu368.

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Barnable, Patrick, Giulia Calenda, Thierry Bonnaire, Radhika Menon, Keith Levendosky, Agegnehu Gettie, James Blanchard, et al. "MIV-150/Zinc Acetate Gel Inhibits Cell-Associated Simian-Human Immunodeficiency Virus Reverse Transcriptase Infection in a Macaque Vaginal Explant Model." Antimicrobial Agents and Chemotherapy 59, no. 7 (April 13, 2015): 3829–37. http://dx.doi.org/10.1128/aac.00073-15.

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ABSTRACTThe transmission of both cell-free and cell-associated immunodeficiency viruses has been demonstrated directly in multiple animal species and possibly occurs in humans, as suggested by genotyping of the infecting human immunodeficiency virus (HIV) in acutely infected women and in semen from their partners. Therefore, a microbicide may need to block both mechanisms of HIV transmission to achieve maximum efficacy. To date, most of the preclinical evaluation of candidate microbicides has been performed using cell-free HIV. New models of mucosal transmission of cell-associated HIV are needed to evaluate candidate microbicide performance. The MIV-150/zinc acetate/carrageenan (MZC) gel protects Depo-Provera-treated macaques against cell-free simian-human immunodeficiency virus reverse transcriptase (SHIV-RT) infection when applied vaginally up to 8 h before challenge. We recently demonstrated the potent activity of MZC gel against cell-free SHIV-RT in macaque vaginal explants. In the current study, we established a cell-associated SHIV-RT infection model of macaque vaginal tissues and tested the activity of MZC gel in this model. MZC gel protected tissues against cell-associated SHIV-RT infection when present at the time of viral exposure or when applied up to 4 days prior to viral challenge. These data support clinical testing of the MZC gel. Overall, ourex vivomodel of cell-associated SHIV-RT infection in macaque vaginal mucosa complements the cell-free infection models, providing tools for prioritization of products that block both modes of HIV transmission.

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Panfil, Amanda R., Jacob J. Al-Saleem, and Patrick L. Green. "Animal Models Utilized in HTLV-1 Research." Virology: Research and Treatment 4 (January 2013): VRT.S12140. http://dx.doi.org/10.4137/vrt.s12140.

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Since the isolation and discovery of human T-cell leukemia virus type 1 (HTLV-1) over 30 years ago, researchers have utilized animal models to study HTLV-1 transmission, viral persistence, virus-elicited immune responses, and HTLV-1-associated disease development (ATL, HAM/TSP). Non-human primates, rabbits, rats, and mice have all been used to help understand HTLV-1 biology and disease progression. Non-human primates offer a model system that is phylogenetically similar to humans for examining viral persistence. Viral transmission, persistence, and immune responses have been widely studied using New Zealand White rabbits. The advent of molecular clones of HTLV-1 has offered the opportunity to assess the importance of various viral genes in rabbits, non-human primates, and mice. Additionally, over-expression of viral genes using transgenic mice has helped uncover the importance of Tax and Hbz in the induction of lymphoma and other lymphocyte-mediated diseases. HTLV-1 inoculation of certain strains of rats results in histopathological features and clinical symptoms similar to that of humans with HAM/TSP. Transplantation of certain types of ATL cell lines in immunocompromised mice results in lymphoma. Recently, “humanized” mice have been used to model ATL development for the first time. Not all HTLV-1 animal models develop disease and those that do vary in consistency depending on the type of monkey, strain of rat, or even type of ATL cell line used. However, the progress made using animal models cannot be understated as it has led to insights into the mechanisms regulating viral replication, viral persistence, disease development, and, most importantly, model systems to test disease treatments.

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Rai, Mohammad Ali, Jason E. Hammonds, Paul Spearman, and Paul Spearman. "2518. Development And Characterization Of Human Microglial Models To Elucidate HIV Transmission Events And Pathogenesis." Open Forum Infectious Diseases 6, Supplement_2 (October 2019): S874—S875. http://dx.doi.org/10.1093/ofid/ofz360.2196.

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Abstract Background HIV-associated neurocognitive disorders cause significant morbidity and mortality despite the advent of antiretroviral therapy. An understanding of fundamental mechanisms underlying HIV infection and transmission events in the central nervous system (CNS) is needed. Microglia are resident myeloid cells that are readily infected by HIV and may constitute a CNS reservoir. We evaluated and compared existing microglial cell lines and primary cell-derived microglia as potential model systems for studying HIV-microglia interactions. Methods We cultured two immortalized human microglial lines (HMC3, C20) and developed two primary microglial models: induced microglia (iMG) derived from primary human monocytes; and microglial-like cells (iMGL) differentiated from induced pluripotent stem cells (iPSCs). We compared these four microglial cell types to commercially available fetal microglia (PM) for a microglial comparator, and monocyte-derived macrophages as a non-microglial comparator cell. Each cell type was evaluated for the presence of typical myeloid and microglia-specific markers by flow cytometry and immunofluorescence microscopy. HIV infection was performed using macrophage-tropic HIV or VSV-G-pseudotyped HIV. Results After differentiation, the iMG and iMGL displayed characteristic microglial morphology: a spindle shape and a reduction in the central body, along with ramified cell processes. Flow cytometry revealed significant differences in surface markers among the cell types. iMG and iMGL displayed CD11b, CD45, CXCR4, CCR5 and lack of expression of CD4 and CX3CR1. In contrast, HMC3, C20, and PM were negative for CD11b, CD45, CX3CR1, CD4, CXCR4. Immunostaining showed that iMG and iMGL were positive for microglial markers TMEM119 and P2RY12. RNA Seq analysis is currently underway to determine gene expression differences between the microglial cell lines and our microglia models. In preliminary results, iMG and iMGL were both readily infected with HIV, and comparison with other lines is ongoing. Conclusion There is no standard model available for defining the molecular and cellular events involved in HIV infection of microglia. Significant differences in microgial markers and in HIV receptor and coreceptor levels were noted in this study. iMG and iMGL appear to be viable microglial models susceptible to HIV infection. Disclosures All authors: No reported disclosures.

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Ahmed, Afzal, Satish V. Ukkusuri, Shahrukh Raza Mirza, and Ausaja Hassan. "Width-Based Cell Transmission Model for Heterogeneous and Undisciplined Traffic Streams." Transportation Research Record: Journal of the Transportation Research Board 2673, no. 5 (April 12, 2019): 682–92. http://dx.doi.org/10.1177/0361198119838841.

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Traffic streams in many developing countries consist of various modes of transport, with high heterogeneity in driver behavior. Modeling these types of traffic streams, in which traffic rules (speed limit, lane discipline, etc.) are not strictly followed, is a complex task. A review of the existing literature shows that there is a lack of traffic flow models that model the behavior of heterogeneous and undisciplined traffic streams. Like other undisciplined traffic streams, there are no speed limits (hence no speed enforcement) on most of the roads in Karachi, Pakistan. Lane discipline is also not observed by drivers, which results in a varying number of traffic lanes on a road. Therefore, most of the existing traffic flow models/simulation packages developed for disciplined traffic streams cannot appropriately model traffic streams without lane discipline. This research proposes a width-based cell transmission model (WCTM) by developing a fundamental flow-density diagram whose parameters are a function of the road width. Extensive field data have been collected from a selected arterial in Karachi for development of the fundamental traffic flow diagram. The values of the computed parameters are significantly different than the values reported in the literature. The piecewise-linear flow-density relation is developed by optimally estimating the breakpoints. Results show that the quadrilateral and pentagonal-shaped fundamental diagrams fit better with the collected data in comparison with the triangular-shaped fundamental diagram. The proposed WCTM is applied to selected segments of an arterial and results show that the WCTM was able to accurately model different traffic conditions.

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Bernard-Stoecklin, S., C. Gommet, M. Cavarelli, and R. Le Grand. "Nonhuman Primate Models for Cell-Associated Simian Immunodeficiency Virus Transmission: The Need to Better Understand the Complexity of HIV Mucosal Transmission." Journal of Infectious Diseases 210, suppl 3 (November 20, 2014): S660—S666. http://dx.doi.org/10.1093/infdis/jiu536.

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Lundgren, Erik, Ethan Romero-Severson, Jan Albert, and Thomas Leitner. "Combining biomarker and virus phylogenetic models improves HIV-1 epidemiological source identification." PLOS Computational Biology 18, no. 8 (August 26, 2022): e1009741. http://dx.doi.org/10.1371/journal.pcbi.1009741.

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To identify and stop active HIV transmission chains new epidemiological techniques are needed. Here, we describe the development of a multi-biomarker augmentation to phylogenetic inference of the underlying transmission history in a local population. HIV biomarkers are measurable biological quantities that have some relationship to the amount of time someone has been infected with HIV. To train our model, we used five biomarkers based on real data from serological assays, HIV sequence data, and target cell counts in longitudinally followed, untreated patients with known infection times. The biomarkers were modeled with a mixed effects framework to allow for patient specific variation and general trends, and fit to patient data using Markov Chain Monte Carlo (MCMC) methods. Subsequently, the density of the unobserved infection time conditional on observed biomarkers were obtained by integrating out the random effects from the model fit. This probabilistic information about infection times was incorporated into the likelihood function for the transmission history and phylogenetic tree reconstruction, informed by the HIV sequence data. To critically test our methodology, we developed a coalescent-based simulation framework that generates phylogenies and biomarkers given a specific or general transmission history. Testing on many epidemiological scenarios showed that biomarker augmented phylogenetics can reach 90% accuracy under idealized situations. Under realistic within-host HIV-1 evolution, involving substantial within-host diversification and frequent transmission of multiple lineages, the average accuracy was at about 50% in transmission clusters involving 5–50 hosts. Realistic biomarker data added on average 16 percentage points over using the phylogeny alone. Using more biomarkers improved the performance. Shorter temporal spacing between transmission events and increased transmission heterogeneity reduced reconstruction accuracy, but larger clusters were not harder to get right. More sequence data per infected host also improved accuracy. We show that the method is robust to incomplete sampling and that adding biomarkers improves reconstructions of real HIV-1 transmission histories. The technology presented here could allow for better prevention programs by providing data for locally informed and tailored strategies.

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Lu, Shoufeng, Shiqiang Dai, and Ximin Liu. "A discrete traffic kinetic model – integrating the lagged cell transmission and continuous traffic kinetic models." Transportation Research Part C: Emerging Technologies 19, no. 2 (April 2011): 196–205. http://dx.doi.org/10.1016/j.trc.2010.05.007.

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Abdullah, Saifuddin, and Dr Fuad Al-Najjar. "A Collective Statistical Analysis of Outdoor Path Loss Models." INTERNATIONAL JOURNAL OF COMPUTERS & TECHNOLOGY 3, no. 1 (August 1, 2012): 6–10. http://dx.doi.org/10.24297/ijct.v3i1a.2720.

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This study encompasses nine path loss models (Erceg-Greenstein, Green-Obaidat, COST Hata, Hata Urban, Hata Rural, Hata Suburban, SUI, Egli and ECC-33) which were programmed on Python and studied for their results in an urban architecture (translated by higher attenuation variables) at 950 MHz and 1800 MHz. The results obtained showed that increasing the transmission antenna height with the increasing distance not only lowers down the path loss readings, but also shows that the standard deviation between the results of studied path loss models increases with the increasing transmission antenna height and increasing distance at both 950 MHz and 1800 MHz systems, especially when transmission antenna height crosses the GSM standard of 40 meters and cell-radius exceeds the limit of 20 kilometers. Moreover, it is also observed that at both 950 MHz and 1800 MHz, the path loss readings of all the models disperse from their collective mean between 1 and 10 Km, but tend converge afterwards (i.e. from 10 to 40 Km and onwards) towards their mean, which indicates that path loss readings of the urban models tend to follow either a single convergence point on large distances or reach their maximum threshold level (a level from which their readings cannot exceed or differ from each other significantly).

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Sethi, Shneh, Kristen M. Kerksiek, Thomas Brocker, and Hans Kretzschmar. "Role of the CD8+ Dendritic Cell Subset in Transmission of Prions." Journal of Virology 81, no. 9 (February 14, 2007): 4877–80. http://dx.doi.org/10.1128/jvi.02345-06.

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ABSTRACT Controversial results have been observed in mouse models regarding the role of lymphoid tissues in prion pathogenesis. To investigate the role of dendritic cells (DC), we used a transgenic mouse model. In this model (CD11c-N17Rac1), a significant reduction of CD8+ CD11chi DC has been described, and the remaining CD8+ DC demonstrate a reduced capacity for the uptake of apoptotic cells. After intraperitoneal prion infection, significantly longer incubation times were observed in CD11c-N17Rac1 mice than in controls, indicating that a defect in CD8+ CD11chi DC significantly impedes neuroinvasion after intraperitoneal infection. In contrast, no distinct differences were observed between CD11c-N17Rac1 mice and controls after oral infection. This provides evidence that oral and intraperitoneal prion infections differ in lymphoreticular requirements.

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Raezah, Aeshah A., Ahmed M. Elaiw, and Badria S. Alofi. "Global Properties of Latent Virus Dynamics Models with Immune Impairment and Two Routes of Infection." High-Throughput 8, no. 2 (June 3, 2019): 16. http://dx.doi.org/10.3390/ht8020016.

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This paper studies the global stability of viral infection models with CTL immune impairment. We incorporate both productively and latently infected cells. The models integrate two routes of transmission, cell-to-cell and virus-to-cell. In the second model, saturated virus–cell and cell–cell incidence rates are considered. The basic reproduction number is derived and two steady states are calculated. We first establish the nonnegativity and boundedness of the solutions of the system, then we investigate the global stability of the steady states. We utilize the Lyapunov method to prove the global stability of the two steady states. We support our theorems by numerical simulations.

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Liu, Qun. "Analysis of a stochastic HIV model with cell-to-cell transmission and Ornstein–Uhlenbeck process." Journal of Mathematical Physics 64, no. 1 (January 1, 2023): 012702. http://dx.doi.org/10.1063/5.0127775.

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In this paper, we establish and analyze a stochastic human immunodeficiency virus model with both virus-to-cell and cell-to-cell transmissions and Ornstein–Uhlenbeck process, in which we suppose that the virus-to-cell infection rate and the cell-to-cell infection rate satisfy the Ornstein–Uhlenbeck process. First, we validate that there exists a unique global solution to the stochastic model with any initial value. Then, we adopt a stochastic Lyapunov function technique to develop sufficient criteria for the existence of a stationary distribution of positive solutions to the stochastic system, which reflects the strong persistence of all CD4+ T cells and free viruses. In particular, under the same conditions as the existence of a stationary distribution, we obtain the specific form of the probability density around the quasi-chronic infection equilibrium of the stochastic system. Finally, numerical simulations are conducted to validate these analytical results. Our results suggest that the methods used in this paper can be applied to study other viral infection models in which the infected CD4+ T cells are divided into latently infected and actively infected subgroups.

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Yadav, Kush Kumar, and Scott P. Kenney. "Animal Models for Studying Congenital Transmission of Hepatitis E Virus." Microorganisms 11, no. 3 (February 28, 2023): 618. http://dx.doi.org/10.3390/microorganisms11030618.

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One of the most intriguing issues in the hepatitis E virus (HEV) field is the significant increase in mortality rates of the mother and fetus when infection occurs in the second and third trimesters of gestation. A virus that is normally self-limiting and has a mortality rate of less than one percent in otherwise healthy individuals steeply rises by up to 30% in these pregnant populations. Answering this pivotal question has not been a simple task. HEV, in general, has been a difficult pathogen to understand in the laboratory setting. A historical lack of ability to efficiently propagate the virus in tissue culture models has led to many molecular aspects of the viral lifecycle being understudied. Although great strides have been made in recent years to adapt viruses to cell culture, this field remains behind other viruses that are much easier to replicate efficiently in vitro. Some of the greatest discoveries regarding HEV have come from using animal models for which naturally occurring strains of HEV have been identified, including pigs and chickens, but key limitations have made animal models imperfect for studying all aspects of human HEV infections. In addition to the difficulties working with HEV, pregnancy is a very complicated biological process with an elaborate interplay between many different host systems, including hormones, cardiovascular, kidneys, respiratory, gastrointestinal, epithelial, liver, metabolic, immune, and others. Significant differences between the timing and interplay of these systems are notable between species, and making direct comparisons between animals and humans can be difficult at times. No simple answer exists as to how HEV enhances mortality in pregnant populations. One of the best approaches to studying HEV in pregnancy is likely a combinatorial approach that uses the best combination of emerging in vitro and in vivo systems while accounting for the deficiencies that are present in each model. This review describes many of the current HEV animal model systems and the strengths and weaknesses of each as they apply to HEV pregnancy-associated mortality. We consider factors that are critical to analyzing HEV infection within the host and how, despite no perfect animal model for human pregnancy mortality existing, recent developments in HEV models, both in vitro and in vivo, are advancing our overall understanding of HEV in the pregnant host.

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Asif, Rao Muhammad, Mustafa Shakir, Ateeq Ur Rehman, Muhammad Shafiq, Rehan Ali Khan, and Wali Ullah Khan. "Performance Evaluation of Spectral Efficiency for Uplink and Downlink Multi-Cell Massive MIMO Systems." Journal of Sensors 2022 (June 30, 2022): 1–12. http://dx.doi.org/10.1155/2022/7205687.

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Massive multiple-input and multiple-output (MIMO) systems have become the most persuasive technology for 5G as it increased the energy efficiency gigantically as compared to other wireless communication systems. Being the most vibrant research technology in the communication sector, this research work is based on the optimal model development of energy-efficient massive MIMO systems. The proposed model is a realistic model that augmented the spectral efficiency (SE) of massive MIMO systems where a multi-cell model scenario is considered. Channel estimation is carried out at the base stations (BSs) based on uplink (UL) transmission while the minimum mean-squared error (MMSE), Element-wise MMSE, and Least-square (LS) estimators are used for the estimation. We analyze the achievable SE of the UL based on the MMSE channel estimator with different receive combining schemes. Moreover, the downlink (DL) transmission model is also modelled with different precoding schemes by taking the same vectors used in combining schemes. The simulation results show a significant improvement in spectral efficiency by developing UL and DL transmission models and also realized that the average sum of SE per cell can be improved by optimized MMSE channel estimation, installing multiple BS antennas, and serving multiple UEs per cell. The findings of this work specify that the massive MIMO system can be developed by optimizing the channel estimation for the augmentation of SE in UL and DL transmissions. Conclusively, it can be summarized that some complex computations of MMSE channel estimators can enhance the average sum of SE per cell as per the results verified in this model.

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Hattaf, Khalid, and Noura Yousfi. "Qualitative Analysis of a Generalized Virus Dynamics Model with Both Modes of Transmission and Distributed Delays." International Journal of Differential Equations 2018 (2018): 1–7. http://dx.doi.org/10.1155/2018/9818372.

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We propose a generalized virus dynamics model with distributed delays and both modes of transmission, one by virus-to-cell infection and the other by cell-to-cell transfer. In the proposed model, the distributed delays describe (i) the time needed for infected cells to produce new virions and (ii) the time necessary for the newly produced virions to become mature and infectious. In addition, the infection transmission process is modeled by general incidence functions for both modes. Furthermore, the qualitative analysis of the model is rigorously established and many known viral infection models with discrete and distributed delays are extended and improved.

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Sun, Zhifeng, Paul W. Denton, Jacob D. Estes, Florence A. Othieno, Bangdong L. Wei, Anja K. Wege, Michael W. Melkus, et al. "Intrarectal transmission, systemic infection, and CD4+ T cell depletion in humanized mice infected with HIV-1." Journal of Experimental Medicine 204, no. 4 (March 26, 2007): 705–14. http://dx.doi.org/10.1084/jem.20062411.

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Intrarectal infection between men who have sex with men represents a predominant form of human immunodeficiency virus (HIV) transmission in developed countries. Currently there are no adequate small animal models that recapitulate intrarectal HIV transmission. Here we demonstrate that human lymphocytes generated in situ from hematopoietic stem cells reconstitute the gastrointestinal tract of humanized mice with human CD4+ T cells rendering them susceptible to intrarectal HIV transmission. HIV infection after a single intrarectal inoculation results in systemic infection with depletion of CD4+ T cells in gut-associated lymphoid tissue and other pathologic sequela that closely mimics those observed in HIV infected humans. This novel model provides the basis for the development and evaluation of novel approaches aimed at immune reconstitution of human gut-associated lymphoid tissue and for the development, testing, and implementation of microbicides to prevent intrarectal HIV-1 transmission.

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Donaldson, L. A. "A THREE-DIMENSIONAL COMPUTER MODEL OF THE TRACHEID CELL WALL AS A TOOL FOR INTERPRETATION OF WOOD CELL WALL ULTRASTRUCTURE." IAWA Journal 22, no. 3 (2001): 213–33. http://dx.doi.org/10.1163/22941932-90000280.

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Three-dimensional computer models were used to simulate transmission electron micrographs in order to determine the effects of changes in microfibril orientation and arrangement on the appearance of ultrastructural images based on thin sections. It is shown that the tangential fibrillar texture commonly associated with wood cell walls results not from individual microfibrils arranged in tangential lamellae but from overlapping of adjacent microfibrils irrespective of their arrangement. The tangential lamellae observed in transmission electron micrographs of wood cell walls do not necessarily reflect the underlying nanostructure of the wall. Tangential textures can occur irrespective of the arrangement of microfibrils in tangential, radial or random patterns as a direct result of the helical organisation of the cell wall. Comparison between model images and high resolution micrographs suggests that microfibrils are arranged randomly in weakly defined clusters, with perhaps varying amounts of tangential or radial organisation.

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Raezah, Aeshah A., Elsayed Dahy, E. Kh Elnahary, and Shaimaa A. Azoz. "Stability of HIV-1 Dynamics Models with Viral and Cellular Infections in the Presence of Macrophages." Axioms 12, no. 7 (June 21, 2023): 617. http://dx.doi.org/10.3390/axioms12070617.

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In this research work, we suggest two mathematical models that take into account (i) two categories of target cells, CD4+T cells and macrophages, and (ii) two modes of infection transmissions, the direct virus-to-cell (VTC) method and cell-to-cell (CTC) infection transmission, where CTC is an effective method of spreading human immunodeficiency virus type-1 (HIV-1), as with the VTC method. The second model incorporates four time delays. In both models, the presence of a bounded and positive solution of the biological model is investigated. The existence conditions of all equilibria are established. The basic reproduction number R0 that identifies a disease index is obtained. Lyapunov functions are utilized to verify the global stability of all equilibria. The theoretical findings are verified through numerical simulations. According to the outcomes, the trajectories of the solutions approach the infection-free equilibrium and infection-present equilibrium when R0≤1 and R0>1, respectively. Further, we study the sensitivity analysis to investigate how the values of all the parameters of the suggested model affect R0 for given data. We discuss the impact of the time delay on HIV-1 progression. We find that a longer time delay results in suppression of the HIV-1 infection and vice versa.

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Zhang, Zhao, Brian Wolshon, and Vinayak V. Dixit. "Integration of a cell transmission model and macroscopic fundamental diagram: Network aggregation for dynamic traffic models." Transportation Research Part C: Emerging Technologies 55 (June 2015): 298–309. http://dx.doi.org/10.1016/j.trc.2015.03.040.

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Maher, Mike. "A comparison of the use of the cell transmission and platoon dispersion models in TRANSYT 13." Transportation Planning and Technology 34, no. 1 (February 2011): 71–85. http://dx.doi.org/10.1080/03081060.2011.530830.

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Rodriguez Fernandez, Veronica, Giovanni Casini, and Fabrizio Bruschi. "Ocular Toxoplasmosis: Mechanisms of Retinal Infection and Experimental Models." Parasitologia 1, no. 2 (April 15, 2021): 50–60. http://dx.doi.org/10.3390/parasitologia1020007.

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Ocular toxoplasmosis (OT) is caused by the parasite Toxoplasma gondii and affects many individuals throughout the world. Infection may occur through congenital or acquired routes. The parasites enter the blood circulation and reach both the retina and the retinal pigment epithelium, where they may cause cell damage and cell death. Different routes of access are used by T. gondii to reach the retina through the retinal endothelium: by transmission inside leukocytes, as free parasites through a paracellular route, or after endothelial cell infection. A main feature of OT is the induction of an important inflammatory state, and the course of infection has been shown to be influenced by the host immunogenetics. On the other hand, there is evidence that the T. gondii phenotype also has an impact on the distribution of the pathology in different areas. Although considerable knowledge has been acquired on OT, a deeper knowledge of its mechanisms is necessary to provide new, more targeted treatment strategies. In particular, in addition to in vitro and in vivo experimental models, organotypic, ex vivo retinal explants may be useful in this direction.

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Ye, Dong, Kenneth A. Dawson, and Iseult Lynch. "A TEM protocol for quality assurance of in vitro cellular barrier models and its application to the assessment of nanoparticle transport mechanisms across barriers." Analyst 140, no. 1 (2015): 83–97. http://dx.doi.org/10.1039/c4an01276c.

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Kocan, Richard M. "Transmission models for the fish pathogen Ichthyophonus: synthesis of field observations and empirical studies." Canadian Journal of Fisheries and Aquatic Sciences 76, no. 4 (April 2019): 636–42. http://dx.doi.org/10.1139/cjfas-2018-0166.

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Empirical studies have demonstrated that Ichthyophonus is transmitted among piscivores via consumption of infected prey; however, this unidirectional mode of transmission from small to large fish cannot sustain Ichthyophonus within a population. To circumvent this problem, Ichthyophonus evolved an infective waterborne cell that has been shown to infect both fresh- and saltwater fish. Successful transmission of Ichthyophonus via a waterborne stage is linked to the proximity of infected and susceptible individuals, a condition met when the two groups occupy the same habitat. It is posited that this occurs during annual inshore migrations when herring (Clupea spp.) enter areas occupied by infected demersal predators. A plausible transmission scenario is that during inshore excursions, planktivores are exposed to infective waterborne cells shed by demersal piscivores. Once planktivores are infected, the parasite is recycled when consumed by predators. This model is supported by reports of ichthyophoniasis increasing in herring populations at the time of inshore migration. The possible role of an intermediate host for Ichthyophonus, as well as evidence for a free-living stage in its life cycle, is presented.

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Lamond, Nicole, and Nancy Freitag. "Vertical Transmission of Listeria monocytogenes: Probing the Balance between Protection from Pathogens and Fetal Tolerance." Pathogens 7, no. 2 (May 25, 2018): 52. http://dx.doi.org/10.3390/pathogens7020052.

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Protection of the developing fetus from pathogens is one of the many critical roles of the placenta. Listeria monocytogenes is one of a select number of pathogens that can cross the placental barrier and cause significant harm to the fetus, leading to spontaneous abortion, stillbirth, preterm labor, and disseminated neonate infection despite antibiotic treatment. Such severe outcomes serve to highlight the importance of understanding how L. monocytogenes mediates infiltration of the placental barrier. Here, we review what is currently known regarding vertical transmission of L. monocytogenes as a result of cell culture and animal models of infection. In vitro cell culture and organ models have been useful for the identification of L. monocytogenes virulence factors that contribute to placental invasion. Examples include members of the Internalin family of bacterial surface proteins such as Interalin (Inl)A, InlB, and InlP that promote invasion of cells at the maternal-fetal interface. A number of animal models have been used to interrogate L. monocytogenes vertical transmission, including mice, guinea pigs, gerbils, and non-human primates; each of these models has advantages while still not providing a comprehensive understanding of L. monocytogenes invasion of the human placenta and/or fetus. These models do, however, allow for the molecular investigation of the balance between fetal tolerance and immune protection from L. monocytogenes during pregnancy.

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Masoli, Stefano, Alessandra Ottaviani, Stefano Casali, and Egidio D’Angelo. "Cerebellar Golgi cell models predict dendritic processing and mechanisms of synaptic plasticity." PLOS Computational Biology 16, no. 12 (December 30, 2020): e1007937. http://dx.doi.org/10.1371/journal.pcbi.1007937.

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The Golgi cells are the main inhibitory interneurons of the cerebellar granular layer. Although recent works have highlighted the complexity of their dendritic organization and synaptic inputs, the mechanisms through which these neurons integrate complex input patterns remained unknown. Here we have used 8 detailed morphological reconstructions to develop multicompartmental models of Golgi cells, in which Na, Ca, and K channels were distributed along dendrites, soma, axonal initial segment and axon. The models faithfully reproduced a rich pattern of electrophysiological and pharmacological properties and predicted the operating mechanisms of these neurons. Basal dendrites turned out to be more tightly electrically coupled to the axon initial segment than apical dendrites. During synaptic transmission, parallel fibers caused slow Ca-dependent depolarizations in apical dendrites that boosted the axon initial segment encoder and Na-spike backpropagation into basal dendrites, while inhibitory synapses effectively shunted backpropagating currents. This oriented dendritic processing set up a coincidence detector controlling voltage-dependent NMDA receptor unblock in basal dendrites, which, by regulating local calcium influx, may provide the basis for spike-timing dependent plasticity anticipated by theory.

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Tan, Steven J., Alice C. Chang, Sarah M. Anderson, Cayla M. Miller, Louis S. Prahl, David J. Odde, and Alexander R. Dunn. "Regulation and dynamics of force transmission at individual cell-matrix adhesion bonds." Science Advances 6, no. 20 (May 2020): eaax0317. http://dx.doi.org/10.1126/sciadv.aax0317.

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Integrin-based adhesion complexes link the cytoskeleton to the extracellular matrix (ECM) and are central to the construction of multicellular animal tissues. How biological function emerges from the tens to thousands of proteins present within a single adhesion complex remains unclear. We used fluorescent molecular tension sensors to visualize force transmission by individual integrins in living cells. These measurements revealed an underlying functional modularity in which integrin class controlled adhesion size and ECM ligand specificity, while the number and type of connections between integrins and F-actin determined the force per individual integrin. In addition, we found that most integrins existed in a state of near-mechanical equilibrium, a result not predicted by existing models of cytoskeletal force transduction. A revised model that includes reversible cross-links within the F-actin network can account for this result and suggests one means by which cellular mechanical homeostasis can arise at the molecular level.

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Haase, Kristina, and Andrew E. Pelling. "Investigating cell mechanics with atomic force microscopy." Journal of The Royal Society Interface 12, no. 104 (March 2015): 20140970. http://dx.doi.org/10.1098/rsif.2014.0970.

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Transmission of mechanical force is crucial for normal cell development and functioning. However, the process of mechanotransduction cannot be studied in isolation from cell mechanics. Thus, in order to understand how cells ‘feel’, we must first understand how they deform and recover from physical perturbations. Owing to its versatility, atomic force microscopy (AFM) has become a popular tool to study intrinsic cellular mechanical properties. Used to directly manipulate and examine whole and subcellular reactions, AFM allows for top-down and reconstitutive approaches to mechanical characterization. These studies show that the responses of cells and their components are complex, and largely depend on the magnitude and time scale of loading. In this review, we generally describe the mechanotransductive process through discussion of well-known mechanosensors. We then focus on discussion of recent examples where AFM is used to specifically probe the elastic and inelastic responses of single cells undergoing deformation. We present a brief overview of classical and current models often used to characterize observed cellular phenomena in response to force. Both simple mechanistic models and complex nonlinear models have been used to describe the observed cellular behaviours, however a unifying description of cell mechanics has not yet been resolved.

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Ciche, Todd A., Kwi-suk Kim, Bettina Kaufmann-Daszczuk, Ken C. Q. Nguyen, and David H. Hall. "Cell Invasion and Matricide during Photorhabdus luminescens Transmission by Heterorhabditis bacteriophora Nematodes." Applied and Environmental Microbiology 74, no. 8 (February 15, 2008): 2275–87. http://dx.doi.org/10.1128/aem.02646-07.

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ABSTRACT Many animals and plants have symbiotic relationships with beneficial bacteria. Experimentally tractable models are necessary to understand the processes involved in the selective transmission of symbiotic bacteria. One such model is the transmission of the insect-pathogenic bacterial symbionts Photorhabdus spp. by Heterorhabditis bacteriophora infective juvenile (IJ)-stage nematodes. By observing egg-laying behavior and IJ development, it was determined that IJs develop exclusively via intrauterine hatching and matricide (i.e., endotokia matricida). By transiently exposing nematodes to fluorescently labeled symbionts, it was determined that symbionts infect the maternal intestine as a biofilm and then invade and breach the rectal gland epithelium, becoming available to the IJ offspring developing in the pseudocoelom. Cell- and stage-specific infection occurs again in the pre-IJ pharyngeal intestinal valve cells, which helps symbionts to persist as IJs develop and move to a new host. Synchronous with nematode development are changes in symbiont and host behavior (e.g., adherence versus invasion). Thus, Photorhabdus symbionts are maternally transmitted by an elaborate infectious process involving multiple selective steps in order to achieve symbiont-specific transmission.

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Danner, S., H. Benzin, T. Vollbrandt, J. Oder, A. Richter, and C. Kruse. "Quantum Dots Do Not Alter the Differentiation Potential of Pancreatic Stem Cells and Are Distributed Randomly among Daughter Cells." International Journal of Cell Biology 2013 (2013): 1–12. http://dx.doi.org/10.1155/2013/918242.

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With the increasing relevance of cell-based therapies, there is a demand for cell-labeling techniques forin vitroandin vivostudies. For the reasonable tracking of transplanted stem cells in animal models, the usage of quantum dots (QDs) for sensitive cellular imaging has major advances. QDs could be delivered to the cytoplasm of the cells providing intense and stable fluorescence. Although QDs are emerging as favourable nanoparticles for bioimaging, substantial investigations are still required to consider their application for adult stem cells. Therefore, rat pancreatic stem cells (PSCs) were labeled with different concentrations of CdSe quantum dots (Qtracker 605 nanocrystals). The QD labeled PSCs showed normal proliferation and their usual spontaneous differentiation potentialin vitro. The labeling of the cell population was concentration dependent, with increasing cell load from 5 nM QDs to 20 nM QDs. With time-lapse microscopy, we observed that the transmission of the QD particles during cell divisions was random, appearing as equal or unequal transmission to daughter cells. We report here that QDs offered an efficient and nontoxic way to label pancreatic stem cells without genetic modifications. In summary, QD nanocrystals are a promising tool for stem cell labeling and facilitate tracking of transplanted cells in animal models.

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El-Khozondar, H. J., M. Abu-Marasa, R. J. El-Khozondar, M. Elbahri, and S. Zouhdi. "Design of Voltage control Oscillator using Nonlinear Composite Right/Left-Handed Transmission Line." Advanced Electromagnetics 5, no. 1 (March 10, 2016): 15. http://dx.doi.org/10.7716/aem.v5i1.342.

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In the present work, we propose a voltage control oscillator (VCO) at high frequency consists of nonlinear composite right/left-handed transmission line (CRLH-TL) loaded with Resonant Tunneling Diode (RTD). We designed three prototype device examples. The first one consists of one cell with short circuit at the beginning of the cell between ground and patch, and 50 Ω load resistance were added at the end of the cell between ground and patch. The second one is similar to the first prototype but with open circuit at the beginning of the cell instated of short circuit. The third prototype consists of one cell with two 50 Ω load resistances added between ground and patch at the beginning and at the end of the cell. The proposed VCO models are capable of generating oscillations at frequencies between 4.87- 14.9 GHz. In our simulations, we used OrCAD and ADS software to analyze the proposed circuit.

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Pawlyta, Mirosława, Szymon Smykała, Barbara Liszka, and Agata Blacha-Grzechnik. "Transmission Electron Microscopy Observation of the Fuel Cell Catalyst Degradation during the Oxygen Reduction Reaction." Defect and Diffusion Forum 420 (November 14, 2022): 91–100. http://dx.doi.org/10.4028/p-975920.

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Increasing durability of catalysts used in fuel cells is a necessary condition for their widespread commercialization. Fulfilling this condition requires understanding the catalyst degradation mechanism to propose how to reduce it. Transmission electron microscopy can help solve this problem thanks to the fact that it enables direct observation and thus unambiguous interpretation of the processes taking place. For this purpose, Identical Location Transmission Electron Microscopy (IL-TEM) was applied for observations of a commercial catalyst (platinum nanoparticles with a diameter of about 2 nm deposited on Vulcan carbon black) before and after durability tests. Obtained results may contribute to the development of better models of phenomena occurring during cell operation.

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Specke, Volker, Stefan J. Tacke, Klaus Boller, Jochen Schwendemann, and Joachim Denner. "Porcine endogenous retroviruses: in vitro host range and attempts to establish small animal models." Journal of General Virology 82, no. 4 (April 1, 2001): 837–44. http://dx.doi.org/10.1099/0022-1317-82-4-837.

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Using transgenic pigs as the source of cells or organs for xenotransplantation is associated with the risk of porcine endogenous retrovirus (PERV) transmission. Multiple proviruses are integrated into the genome of all pigs, and virus particles, some of which are able to infect human cells, are released from normal pig cells. In order to evaluate the potential risk posed by the transmission of PERVs, in vitro infection studies were performed as a basis for small animal as well as non-human primate models. In vitro infectivity was demonstrated for permanent cell lines and primary cells from a wide range of species. Productive infection was shown using reverse transcriptase (RT) assays and RT–PCR for mink, feline and human kidney cell lines, primary rhesus peripheral blood mononuclear cells (PBMCs), and baboon spleen cells and PBMCs as well as for different human lymphoid and monocyte cell lines and PBMCs. In an attempt to establish a small animal model, naive guinea pigs, non-immunosuppressed rats, rats immunosuppressed by cyclosporin-A and immunosuppressed rats treated with cobra venom factor were inoculated with PERVs produced from porcine kidney PK-15 cells, infected human 293 kidney cells and mitogen-stimulated porcine PBMCs. Animals were also inoculated with PERV-producing PK-15 and 293 cells. No antibodies against PERV and no provirus integration were observed in any of the treated animals. This suggests that productive infection of these animals did not occur in this experimental setting.

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DUNN, A. M., R. S. TERRY, and D. E. TANEYHILL. "Within-host transmission strategies of transovarial, feminizing parasites of Gammarus duebeni." Parasitology 117, no. 1 (July 1998): 21–30. http://dx.doi.org/10.1017/s0031182098002753.

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The amphipod Gammarus duebeni harbours several species of vertically transmitted, feminizing microsporidian parasites. G. duebeni were collected from 3 localities in the UK. Animals from Budle Bay, Northumberland, were infected with Octosporea effeminans, and those from Millport, Isle of Cumbrae and Fenham Flats, Northumberland were infected with microsporidia of the genus Nosema. We derived expected distributions of parasites per host embryonic cell by modelling parasite transmission as a multitype, Galton–Watson branching process. Parasite prevalence (proportion of females infected) was significantly heterogeneous among localities. Parasite burden in zygotes was much higher for females infected with Nosema than in animals infected with O. effeminans. There was no significant difference between localities in the number of Nosema in the zygotes. Comparison of models and data from 64-cell host embryos showed that the distributions of parasites per cell were consistent with the hypothesis that sorting of parasites into daughter cells is biased for at least 1 cell lineage. Host embryos infected with O. effeminans could expect to contain a growing number of parasites in each cell generation within such biased cell lineages; similar estimates for Nosema predict a decline in the number of parasites per cell within a biased lineage. We discuss the possibility that the 2 species of parasite may be employing different strategies in order to ensure transmission to the next host generation.

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Nielsen, Michael H., Dongsheng Li, Hengzhong Zhang, Shaul Aloni, T. Yong-Jin Han, Cathrine Frandsen, Jong Seto, Jillian F. Banfield, Helmut Cölfen, and James J. De Yoreo. "Investigating Processes of Nanocrystal Formation and Transformation via Liquid Cell TEM." Microscopy and Microanalysis 20, no. 2 (March 14, 2014): 425–36. http://dx.doi.org/10.1017/s1431927614000294.

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AbstractRecent ex situ observations of crystallization in both natural and synthetic systems indicate that the classical models of nucleation and growth are inaccurate. However, in situ observations that can provide direct evidence for alternative models have been lacking due to the limited temporal and spatial resolution of experimental techniques that can observe dynamic processes in a bulk solution. Here we report results from liquid cell transmission electron microscopy studies of nucleation and growth of Au, CaCO3, and iron oxide nanoparticles. We show how these in situ data can be used to obtain direct evidence for the mechanisms underlying nanoparticle crystallization as well as dynamic information that provide constraints on important energetic parameters not available through ex situ methods.

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Journal articles on the topic 'Cell transmission models'

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