Pushforwards of Tilting Sheaves

We investigate the behaviour of tilting sheaves under pushforward by a finite Galois morphism. We determine conditions under which such a pushforward of a tilting sheaf is a tilting sheaf. We then produce some examples of Severi Brauer flag varieties and arithmetic toric varieties in which our method produces a tilting sheaf, adding to the list of positive results in the literature. We also produce some counterexamples to show that such a pushfoward need not be a tilting sheaf.Comment: 21 page

STING-mediated disruption of calcium homeostasis chronically activates ER stress and primes T cell death

STING gain-of-function mutations cause lung disease and T cell cytopenia through unknown mechanisms. Here, we found that these mutants induce chronic activation of ER stress and unfolded protein response (UPR), leading to T cell death by apoptosis in th

A Cytotoxic, Co-operative Interaction Between Energy Deprivation and Glutamate Release From System x\u3csub\u3ec\u3c/sub\u3e\u3csup\u3e−\u3c/sup\u3e Mediates Aglycemic Neuronal Cell Death

The astrocyte cystine/glutamate antiporter (system xc−) contributes substantially to the excitotoxic neuronal cell death facilitated by glucose deprivation. The purpose of this study was to determine the mechanism by which this occurred. Using pure astrocyte cultures, as well as, mixed cortical cell cultures containing both neurons and astrocytes, we found that neither an enhancement in system xc− expression nor activity underlies the excitotoxic effects of aglycemia. In addition, using three separate bioassays, we demonstrate no change in the ability of glucose-deprived astrocytes—either cultured alone or with neurons—to remove glutamate from the extracellular space. Instead, we demonstrate that glucose-deprived cultures are 2 to 3 times more sensitive to the killing effects of glutamate or N-methyl-D-aspartate when compared with their glucose-containing controls. Hence, our results are consistent with the weak excitotoxic hypothesis such that a bioenergetic deficiency, which is measureable in our mixed but not astrocyte cultures, allows normally innocuous concentrations of glutamate to become excitotoxic. Adding to the burgeoning literature detailing the contribution of astrocytes to neuronal injury, we conclude that under our experimental paradigm, a cytotoxic, co-operative interaction between energy deprivation and glutamate release from astrocyte system xc− mediates aglycemic neuronal cell death

Exploring the use of children's literature in upper primary classrooms to foster students' critical thinking skills

The purpose of this research is to find out the use of children’s literature in fostering critical thinking skills in the context of Hong Kong upper primary school classroom. The objectives of this research are to find our how children’s literature are used in local primary schools, how teachers value picture books as a teaching resource and the feasibility of using children’s literature in local primary school classrooms to foster critical thinking skills. This ethnographic study involved experienced English teachers from two local primary schools located in different districts in Hong Kong, which they were interviewed and observed on their classroom practices of using children’s literature in the classroom. The data collected is presented in form of a narrative inquiry, which tells the career journeys of the participants. From the results, it was found that the teachers were constraint by the time, textbooks and lack training in using children’s literature.published_or_final_versionEducationBachelorBachelor of Education in Language Educatio

Placental Mesenchymal Stem Cell-Derived Extracellular Vesicles Promote Myelin Regeneration in an Animal Model of Multiple Sclerosis.

Mesenchymal stem/stromal cells (MSCs) display potent immunomodulatory and regenerative capabilities through the secretion of bioactive factors, such as proteins, cytokines, chemokines as well as the release of extracellular vesicles (EVs). These functional properties of MSCs make them ideal candidates for the treatment of degenerative and inflammatory diseases, including multiple sclerosis (MS). MS is a heterogenous disease that is typically characterized by inflammation, demyelination, gliosis and axonal loss. In the current study, an induced experimental autoimmune encephalomyelitis (EAE) murine model of MS was utilized. At peak disease onset, animals were treated with saline, placenta-derived MSCs (PMSCs), as well as low and high doses of PMSC-EVs. Animals treated with PMSCs and high-dose PMSC-EVs displayed improved motor function outcomes as compared to animals treated with saline. Symptom improvement by PMSCs and PMSC-EVs led to reduced DNA damage in oligodendroglia populations and increased myelination within the spinal cord of treated mice. In vitro data demonstrate that PMSC-EVs promote myelin regeneration by inducing endogenous oligodendrocyte precursor cells to differentiate into mature myelinating oligodendrocytes. These findings support that PMSCs' mechanism of action is mediated by the secretion of EVs. Therefore, PMSC-derived EVs are a feasible alternative to cellular based therapies for MS, as demonstrated in an animal model of the disease

Disentangling the relationship between falls, fear of falling, physical function and walking by applying a socioecological framework to the International Mobility in Aging Study

Introduction:The relationships between falls, fear of falling, poor mobility, and PA avoidance occur in a cyclic, multi-directional fashion. Aim: This study investigates the concomitant associations of fall history, fear of falling, and physical performance (SPPB) on physical activity using a cross-national sample of community-dwelling older adults from middle and high-income countries.Methods:Linear mixed-effects models looking at the influence of individual and environmental factors were used and participants were nested within each study site.Results:Estimated walking minutes was 52% lower for those with low SPPB compared to high SPPB, 20% lower for those with medium level fear of falling compared to low levels, and 50% lower for those with high level fear of falling compared to low levels.Conclusion:An individual’s fear of falling and physical performance may be important to consider when making PA recommendations to older adults regardless of sex, age, and environment

Mutation in mitochondrial complex I ND6 subunit is associated with defective response to hypoxia in human glioma cells

BACKGROUND: Hypoxia-tolerant human glioma cells reduce oxygen consumption rate in response to oxygen deficit, a defense mechanism that contributes to survival under moderately hypoxic conditions. In contrast, hypoxia-sensitive cells lack this ability. As it has been previously shown that hypoxia-tolerant (M006x, M006xLo, M059K) and -sensitive (M010b) glioma cells express differences in mitochondrial function, we investigated whether mitochondrial DNA-encoded mutations are associated with differences in the initial response to oxygen deficit. RESULTS: The mitochondrial genome was sequenced and 23 mtDNA alterations were identified, one of which was an unreported mutation (T-C transition in base pair 14634) in the hypoxia-sensitive cell line, M010b, that resulted in a single amino acid change in the gene encoding the ND6 subunit of NADH:ubiquinone oxidoreductase (Complex I). The T14634C mutation did not abrogate ND6 protein expression, however, M010b cells were more resistant to rotenone, an agent used to screen for Complex I mutations, and adriamycin, an agent activated by redox cycling. The specific function of mtDNA-encoded, membrane-embedded Complex I ND subunits is not known at present. Current models suggest that the transmembrane arm of Complex I may serve as a conformationally driven proton channel. As cellular respiration is regulated, in part, by proton flux, we used homology-based modeling and computational molecular biology to predict the 3D structure of the wild type and mutated ND6 proteins. These models predict that the T14634C mutation alters the structure and orientation of the trans-membrane helices of the ND6 protein. CONCLUSION: Complex I ND subunits are mutational hot spots in tumor mtDNA. Genetic changes that alter Complex I structure and function may alter a cell's ability to respond to oxygen deficit and consolidate hypoxia rescue mechanisms, and may contribute to resistance to chemotherapeutic agents that require redox cycling for activation

Poverty alleviation and policy dynamics in Hong Kong : a study of the community care fund

published_or_final_versionPolitics and Public AdministrationMasterMaster of Public Administratio