Family Mathematics Night

The purpose of this project was to develop a family mathematics night program that would encourage parental involvement in mathematics education thus, enhancing student achievement in mathematics. Parents attending the program would: (a) become familiar with the current mathematics program used by their children; (b) learn mathematics games to play at home with their children; and (c) be introduced to various child appropriate, mathematics web sites on the Internet. Much of the material presented was recapped in a miniguide to fourth grade mathematics that was given to all the families. This guide is a tool for the parents to use at home while helping their children with mathematics. The project was reviewed by master teachers to ensure that the project goals were attained. Limitations to the project and suggestions for further study were included in Chapter Five

Andrew Johnson and the Failure of Moderate Reconstruction

This paper represents an attempt to determine why Andrew Johnson\u27s moderate policy for the reconstruction of the South failed. Because the paper is a study of Andrew Johnson, the politician, it dwells primarily only upon the political climate of 1865--although the importance of the social and economic changes occurring during reconstruction is recognized, they are herein treated only incidentally. In essence, the paper demonstrates the defeat of a politician. It is, furthermore, the contention of the paper that moderate reconstruction failed because of the ineffectiveness of its administrator--Andrew Johnson--not because of cabalistic intrigues hatched by those whom F.B. Simkins scoffingly calls Carlyle\u27s wild-eyed conspirators. Johnson was no helpless victim of the unconquerable radical forces about him, but became hopelessly ensnared in a defeat woven by his own inflexible, egotistical temperament which resulted in both political misjudgments and incompetent political maneuvers

The Biochemical Characterization Of Neuronal K+ Channel N-Glycans And Their Role In Regulating K+ Channel Function

The Kv3 and Kv1 subfamilies of voltage–gated K+ channels are critical components which contribute to action potential repolarization throughout the central nervous system. Here, it was shown that both absolutely conserved N–glycosylation sites of the Kv3.1, Kv3.3 and Kv3.4 proteins were occupied in the central nervous system of the adult rat by complex oligosaccharides. Additionally, it was demonstrated that the expression patterns of the Kv3 glycoproteins were different from one another throughout the central nervous system. Electrophoretic migration patterns of the Kv3 glycoproteins from different membranes of the central nervous system digested with glycosidases were utilized to identify the attachment of unique sialylated N–glycan structures. An examination of these sialylated N–glycan structures revealed that the Kv3 glycoproteins, along with the Kv1.1, Kv1.2, and Kv1.4 glycoproteins, were terminated with atypical disialyl units. Moreover, at least one of the carbohydrate chains of the Kv3.1, Kv3.3 and Kv3.4 glycoproteins, like Kv3.1 heterologously expressed in B35 cells, was capped with an oligo/polysialic acid unit. Notably, this is the first time that di/oligo/polysialyl units have been shown to be associated with K+ channels. Sialyl residues linked to internal carbohydrate residues were shown to be components of the N–glycans of the Kv1 glycoproteins, as well as the Kv3 glycoproteins and N–CAM. To date, this unusual glycosidic bond for sialyl residues has not been identified on N–glycans. Whole cell current measurements of glycosylated (wild type), unglycosylated mutant (N220Q/N229Q) and partially glycosylated mutant (N220Q and N229Q) Kv3.1 channels heterologously expressed in B35 cells revealed that the glycosylated Kv3.1 protein could favor a subpopulation of channels with fast activation and inactivation rates for inactivating currents. However, this subpopulation was undetectable for the inactivating currents of the unglycosylated and partially glycosylated Kv3.1 channels. Additionally, the noninactivating current type of the glycosylated and partially glycosylated Kv3.1 channels revealed a subpopulation of Kv3.1 channels with fast activation and inactivation rates, as well as with fast activation and slow inactivation. We conclude that the presence of atypical sialylated N–glycans of Kv3 glycoproteins, and perhaps Kv1 glycoproteins, in mammalian brain is critical in modulating the expression of K+ currents at the surface of neurons.Ph.D

The Benedum Collaborative Model of Teacher Education Student Handbook

The College of Human Resources & Education welcomes you as students in the Five-Year Teacher Education Program. You will find that your experiences in the Benedum Collaborative will prepare you well as you begin your work in the teaching profession. Our partnership with the professional development schools in the Collaborative provides the setting for clinical experiences that build on your course work at West Virginia University

Rapid prototype feasibility testing with simulation: Improvements and updates to the Taiwanese “aerosol box”

This article is made available for unrestricted research re-use and secondary analysis in any form or by any means with acknowledgement of the original source. These permissions are granted for the duration of the World Health Organization (WHO) declaration of COVID-19 as a global pandemic

Alternatively activated macrophages promotes necrosis resolution following acute liver injury

Background & Aim Following acetaminophen (APAP) overdose, acute liver injury (ALI) can occur in patients that present too late for N-acetylcysteine treatment, potentially leading to acute liver failure, systemic inflammation, and death. Macrophages influence the progression and resolution of ALI due to their innate immunological function and paracrine activity. Syngeneic primary bone marrow-derived macrophages (BMDMs) were tested as a cell-based therapy in a mouse model of APAP-induced ALI (APAP-ALI). Methods Several phenotypically distinct BMDM populations were delivered intravenously to APAP-ALI mice when hepatic necrosis was established, and then evaluated based on their effects on injury, inflammation, immunity, and regeneration. In vivo phagocytosis assays were used to interrogate the phenotype and function of alternatively activated BMDMs (AAMs) post-injection. Finally, primary human AAMs sourced from healthy volunteers were evaluated in immunocompetent APAP-ALI mice. Results BMDMs rapidly localised to the liver and spleen within 4 h of administration. Injection of AAMs specifically reduced hepatocellular necrosis, HMGB1 translocation, and infiltrating neutrophils following APAP-ALI. AAM delivery also stimulated proliferation in hepatocytes and endothelium, and reduced levels of several circulating proinflammatory cytokines within 24 h. AAMs displayed a high phagocytic activity both in vitro and in injured liver tissue post-injection. Crosstalk with the host innate immune system was demonstrated by reduced infiltrating host Ly6Chi macrophages in AAM-treated mice. Importantly, therapeutic efficacy was partially recapitulated using clinical-grade primary human AAMs in immunocompetent APAP-ALI mice, underscoring the translational potential of these findings. Conclusion We identify that AAMs have value as a cell-based therapy in an experimental model of APAP-ALI. Human AAMs warrant further evaluation as a potential cell-based therapy for APAP overdose patients with established liver injury. Lay summary After an overdose of acetaminophen (paracetamol), some patients present to hospital too late for the current antidote (N-acetylcysteine) to be effective. We tested whether macrophages, an injury-responsive leukocyte that can scavenge dead/dying cells, could serve as a cell-based therapy in an experimental model of acetaminophen overdose. Injection of alternatively activated macrophages rapidly reduced liver injury and reduced several mediators of inflammation. Macrophages show promise to serve as a potential cell-based therapy for acute liver injury

EuroPhenome: a repository for high-throughput mouse phenotyping data.

The broad aim of biomedical science in the postgenomic era is to link genomic and phenotype information to allow deeper understanding of the processes leading from genomic changes to altered phenotype and disease. The EuroPhenome project (http://www.EuroPhenome.org) is a comprehensive resource for raw and annotated high-throughput phenotyping data arising from projects such as EUMODIC. EUMODIC is gathering data from the EMPReSSslim pipeline (http://www.empress.har.mrc.ac.uk/) which is performed on inbred mouse strains and knock-out lines arising from the EUCOMM project. The EuroPhenome interface allows the user to access the data via the phenotype or genotype. It also allows the user to access the data in a variety of ways, including graphical display, statistical analysis and access to the raw data via web services. The raw phenotyping data captured in EuroPhenome is annotated by an annotation pipeline which automatically identifies statistically different mutants from the appropriate baseline and assigns ontology terms for that specific test. Mutant phenotypes can be quickly identified using two EuroPhenome tools: PhenoMap, a graphical representation of statistically relevant phenotypes, and mining for a mutant using ontology terms. To assist with data definition and cross-database comparisons, phenotype data is annotated using combinations of terms from biological ontologies

Tissue coenzyme Q (ubiquinone) and protein concentrations over the life span of the laboratory rat

The coenzyme Q (ubiquinone) concentrations of a number of tissues have been determined over the life span of the male laboratory rat. Coenzyme Q increased between 2 and 18 months and decreased significantly at 25 months in the heart and kidney, and the gastrocnemius, oblique and deep aspect (red) vastus lateralis muscles. The coenzyme Q concentration of liver increased over the life span, while it remained relatively constant in brain, lung, and the superficial aspect (white) of the vastus lateralis muscle. Data are also included for organ weights and protein contents of tissues over the life span. The various roles of coenzyme Q in cellular electron transfer and its regulation, energy conservation in oxidative phosphorylation, and its clinical efficacy in diseases of energy metabolism are discussed. It is hypothesized that coenzyme Q serves as a free radical quencher in the mitochondrion, a major site of free radical formation, in addition to its other roles in cellular energy metabolism, and that its cellular diminution may contribute to the loss of cellular function accompanying ageing.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/25514/1/0000055.pd