Color: Its Basis, Functions, and Importance in the Teaching of Art for Grades 7 & 8

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SIMULATION ANALYSIS OF USMC HIMARS EMPLOYMENT IN THE WESTERN PACIFIC

As a result of renewed focus on great power competition, the United States Marine Corps is currently undergoing a comprehensive force redesign. In accordance with the Commandant’s Planning Guidance and Force Design 2030, this redesign includes an increase of 14 rocket artillery batteries while divesting 14 cannon artillery batteries. These changes necessitate study into tactics and capabilities for rocket artillery against a peer threat in the Indo-Pacific region. This thesis implements an efficient design of experiments to simulate over 1.6 million Taiwan invasions using a stochastic, agent-based combat model. Varying tactics and capabilities as input, the model returns measures of effectiveness to serve as the response in metamodels, which are then analyzed for critical factors, interactions, and change points. The analysis provides insight into the principal factors affecting lethality and survivability for ground-based rocket fires. The major findings from this study include the need for increasingly distributed artillery formations, highly mobile launchers that can emplace and displace quickly, and the inadequacy of the unitary warheads currently employed by HIMARS units. Solutions robust to adversary actions and simulation variability can inform wargames and future studies as the Marine Corps continues to adapt in preparation for potential peer conflict.Captain, United States Marine CorpsApproved for public release. Distribution is unlimited

\u3ci\u3eAmblyomma maculatum\u3c/i\u3e SECIS Binding Protein 2 and Putative Selenoprotein P are Indispensable for Pathogen Replication and Tick Fecundity

Selenium, a vital trace element, is incorporated into selenoproteins to produce selenocysteine. Our previous studies have revealed an adaptive co-evolutionary process that has enabled the spotted fever-causing tick-borne pathogen Rickettsia parkeri to survive by manipulating an antioxidant defense system associated with selenium, which includes a full set of selenoproteins and other antioxidants in ticks. Here, we conducted a systemic investigation of SECIS binding protein 2 (SBP2) and putative selenoprotein P (SELENOP) by transcript silencing in adult female Gulf-coast ticks (Amblyomma maculatum). Knockdown of the SBP2 and SELENOP genes depleted the respective transcript levels of these tick selenogenes, and caused differential regulation of other antioxidants. Importantly, the selenium level in the immature and mature tick stages increased significantly after a blood meal, but the selenium level decreased in ticks after the SBP2 and SELENOP knockdowns. Moreover, the SBP2 knockdown significantly impaired both transovarial transmission of R. parkeri to tick eggs and egg hatching. Overall, our data offer new insight into the relationship between the SBP2 selenoprotein synthesis gene and the putative tick SELENOP gene. It also augments our understanding of selenoprotein synthesis, selenium maintenance and utilization, and bacterial colonization of a tick vector

\u3ci\u3eRickettsia parkeri\u3c/i\u3e Colonization in \u3ci\u3eAmbylomma maculatum\u3c/i\u3e: The Role of Superoxide Dismutases

Background The Gulf Coast tick (Amblyomma maculatum) is an arthropod vector of Rickettsia parkeri, the causative agent of American boutonneuse fever and an infectious agent of public health significance. In this study, we evaluated the biological significance of the superoxide dismutases (SODs) of A. maculatum in hematophagy and R. parkeri colonization within the tick host. Methods An RNA interference approach was used to measure the functional roles of tick SODs (Cu/Zn-SOD and Mn-SOD) in R. parkeri colonization of the tick vector. Total microbial load, R. parkeri infection rate, and compensatory mechanisms by tick genes were examined using quantitative polymerase chain reaction (PCR) and quantitative reverse-transcriptase PCR assays. SOD enzymatic activity assays and malondialdehyde (MDA) lipid peroxidation were employed to determine the redox states in the tick tissues. Results Knockdown of the Cu/Zn-SOD gene caused the upregulation of Mn-SOD in transcript levels. Single and dual knockdowns of the SOD genes caused an increase in MDA lipid peroxidation while SOD enzymatic activities did not show a significant change. Mn-SOD knockdown resulted in a substantial increase in the microbial load; however, Cu/Zn-SOD transcript depletion prompted an upsurge in the midgut bacterial load, and significantly decreased the bacterial load in salivary gland tissues. Additionally, Cu/Zn-SOD transcript silencing led to significantly fewer R. parkeri DNA copy numbers in both tick tissues (midguts and salivary glands). Conclusions SOD enzymes play an important function in the regulation of bacterial communities associated with tick vectors and also in the defense mechanisms against the damage caused by reactive oxygen species within the tick. Knockdown experiments increased the levels of total oxidative stress in ticks, revealing the interplay between SOD isozymes that results in the transcriptional regulation of tick antioxidants. Moreover, the tick\u27s Cu/Zn-SOD aids in the colonization of R. parkeri in tick tissues providing evidence of A. maculatum\u27s vectorial success for a spotted fever group rickettsial pathogen

Investigating equine host barriers to infection with influenza A viruses

Influenza A viruses (IAVs) are significant pathogens of humans and animals whose main natural host is considered to be wild waterfowl. IAVs have jumped the species barrier on multiple occasions, sometimes with devastating consequences. Successful infection and onward transmission (i.e. viral emergence) requires highly specific interactions between virus and host proteins. However, how an avian virus adapts to a mammalian host to establish as a novel pathogen after initial interspecies transmission is not yet clear. It was hypothesized that adaptation of an avian virus to mammals would involve changes in virus-host interactions that would result in more efficient viral replication and counteraction of immune responses. To test this hypothesis this thesis firstly describes the characterization of an equine dermal cell line (E.Derm) for the study of infection with EIVs. A panel of H3N8 AIVs was selected to investigate how equine host barriers affect the replication kinetics of distinct viruses. Finally, the transcriptome of the equine cells was investigated after infection with two evolutionary distinct H3N8 equine influenza viruses (H3N8 EIVs), and treatment with interferon-alpha (IFN-α). H3N8 EIV is an avian-origin virus that emerged in 1960s and has been circulating in horses for over 50 years, thus providing a natural model system to study the interspecies transmission and post-transfer adaptation of an avian influenza virus to a mammalian host. To examine the cellular response to infection, equine dermal cells (E.Derm) were infected with either A/equine/Uruguay/63 or A/equine/Ohio/2003. Total RNA was extracted at 4 and 24 hours post-infection for RNA sequencing and downstream transcriptomics analysis. Mock-infected cells and interferon-treated cells were also included for comparison purposes. RNA-seq data were analysed using CuffDiff2 to identify differentially expressed (DE) genes between samples. Ingenuity Pathway Analysis was used to determine the intracellular pathways in which DE genes were involved. The results showed clear differences on the intracellular pathways affected between the viruses, which were especially evident during the eclipse phase of virus replication. Distinct intracellular pathways were identified as important for EIV adaptation to the horse, which in turn could be employed by other avian influenza viruses to establish in mammals

The Tick Endosymbiont \u3ci\u3eCandidatus\u3c/i\u3e Midichloria Mitochondrii and Selenoproteins are Essential for the Growth of \u3ci\u3eRickettsia parkeri\u3c/i\u3e in the Gulf Coast Tick Vector

Background Pathogen colonization inside tick tissues is a significant aspect of the overall competence of a vector. Amblyomma maculatum is a competent vector of the spotted fever group rickettsiae, Rickettsia parkeri. When R. parkeri colonizes its tick host, it has the opportunity to dynamically interact with not just its host but with the endosymbionts living within it, and this enables it to modulate the tick’s defenses by regulating tick gene expression. The microbiome in A. maculatum is dominated by two endosymbiont microbes: a Francisella-like endosymbiont (FLE) and CandidatusMidichloria mitochondrii (CMM). A range of selenium-containing proteins (selenoproteins) in A. maculatum ticks protects them from oxidative stress during blood feeding and pathogen infections. Here, we investigated rickettsial multiplication in the presence of tick endosymbionts and characterized the functional significance of selenoproteins during R. parkeri replication in the tick. Results FLE and CMM were quantified throughout the tick life stages by quantitative PCR in R. parkeri-infected and uninfected ticks. R. parkeri infection was found to decrease the FLE numbers but CMM thrived across the tick life cycle. Our qRT-PCR analysis indicated that the transcripts of genes with functions related to redox (selenogenes) were upregulated in ticks infected with R. parkeri. Three differentially expressed proteins, selenoprotein M, selenoprotein O, and selenoprotein S were silenced to examine their functional significance during rickettsial replication within the tick tissues. Gene silencing of the target genes was found to impair R. parkeri colonization in the tick vector. Knockdown of the selenogenes triggered a compensatory response from other selenogenes, as observed by changes in gene expression, but oxidative stress levels and endoplasmic reticulum stress inside the ticks were also found to have heightened. Conclusions This study illustrates the potential of this new research model for augmenting our understanding of the pathogen interactions occurring within tick hosts and the important roles that symbionts and various tick factors play in regulating pathogen growth