Person-centred care for demented older adults: a qualitative analysis

published_or_final_versio

A Study of Energy-efficient Routing Supporting Coordinated Sleep Scheduling in Wireless Ad Hoc Networks

A wireless ad hoc network is a collection of wireless computing devices that self-configure to form a network independently of any fixed infrastructure. Many wireless ad hoc network devices such as smartphones and tablets are usually powered by batteries with a limited operation time. This poses a significant challenge to the design of low-power network protocols. On one hand, energy-efficient routing protocols are widely discussed to reduce the end-to-end transmission energy by controlling the transmission power at senders. Recently, opportunistic routing (OR) has attracted a lot of attention for maximizing energy efficiency by exploiting the gains of multi-receiver diversity. On the other hand, sleep scheduling is commonly adopted as an effective mechanism to further reduce power wasted in overhearing and idle listening. However, the prior work has mainly treated energy-efficient routing and sleep scheduling as two separate tasks, which leads to a serious problem that neither component can fully minimize the network-wide energy consumption. In this thesis, we study how energy-efficient routing can be coordinated with sleep scheduling to increase network-side energy efficiency. We identify a trade-off between the decreased transmit power at senders due to multi-receiver diversity and the increased power at forwarders with the incorporation of coordinated sleep scheduling. Moreover, we provide a comprehensive evaluation of coordinated sleep scheduling impact on energy-efficient routing performance based on a 2-D grid topology and time division multiple access (TDMA) medium access control (MAC). Extensive simulation results demonstrate the effectiveness of the integrated function of coordinated sleep scheduling, significant impact of coordinated sleep scheduling on the energy-efficient routing performance and relationship between the network conditions (in terms of the traffic load and node density) and overall system performance achieved by different energy-efficient routing protocols

25-Hydroxyvitamin D-3 induces osteogenic differentiation of human mesenchymal stem cells

25-Hydroxyvitamin D-3 [25(OH)D-3] has recently been found to be an active hormone. Its biological actions are demonstrated in various cell types. 25(OH)D-3 deficiency results in failure in bone formation and skeletal deformation. Here, we investigated the effect of 25(OH)D-3 on osteogenic differentiation of human mesenchymal stem cells (hMSCs). We also studied the effect of 1 alpha, 25-dihydroxyvitamin D-3[1 alpha,25-(OH)(2)D-3], a metabolite of 25(OH)D-3. One of the vitamin D responsive genes, 25(OH)D-3-24-hydroxylase (cytochrome P450 family 24 subfamily A member 1) mRNA expression is up-regulated by 25(OH)D-3 at 250-500 nM and by 1 alpha, 25-(OH)(2)D-3 at 1-10 nM. 25(OH)D-3 and 1 alpha, 25-(OH)(2)D-3 at a time-dependent manner alter cell morphology towards osteoblast-associated characteristics. The osteogenic markers, alkaline phosphatase, secreted phosphoprotein 1 (osteopontin), and bone gamma-carboxyglutamate protein (osteocalcin) are increased by 25(OH)D-3 and 1 alpha,25-(OH)(2)D-3 in a dose-dependent manner. Finally, mineralisation is significantly increased by 25(OH)D-3 but not by 1 alpha, 25-(OH)(2)D-3. Moreover, we found that hMSCs express very low level of 25(OH)D-3-1 alpha-hydroxylase (cytochrome P450 family 27 subfamily B member 1), and there is no detectable 1 alpha, 25-(OH)(2)D-3 product. Taken together, our findings provide evidence that 25(OH)D-3 at 250-500 nM can induce osteogenic differentiation and that 25(OH)D-3 has great potential for cell-based bone tissue engineering.Peer reviewe

Perpendicular magnetic anisotropy in as-deposited CoFeB/MgO thin films

Fabrication of perpendicularly magnetized ferromagnetic films on various buffer layers, especially on numerous newly discovered spin-orbit torque (SOT) materials to construct energy-efficient spin-orbitronic devices, is a long-standing challenge. Even for the widely used CoFeB/MgO structures, perpendicular magnetic anisotropy (PMA) can only be established on limited buffer layers through post-annealing above 300 {\deg}C. Here, we report that the PMA of CoFeB/MgO films can be established reliably on various buffer layers in the absence of post-annealing. Further results show that precise control of MgO thickness, which determines oxygen diffusion in the underneath CoFeB layer, is the key to obtaining the as-deposited PMA. Interestingly, contrary to previous understanding, post-annealing does not influence the well-established as-deposited PMA significantly but indeed enhances unsaturated PMA with a thick MgO layer by modulating oxygen distributions, rather than crystallinity or Co- and Fe-O bonding. Moreover, our results indicate that oxygen diffusion also plays a critical role in the PMA degradation at high temperature. These results provide a practical approach to build spin-orbitronic devices based on various high-efficient SOT materials.Comment: 15 pages, 4 figure

Theoretical Study of Seal Spring in a Wankel Compressor

The successful fabrication of a miniature Wankel compressor relies on its seal performance.The factors that influence the seal of a miniature Wankel compressor mainly include axial double mechanical seal and apex seals.Axial mechanical seal depends on machining precision on the end face.In the compression cavity, the springs for seal flake on the Wankel rotor put pressure on cylinder ,which generates the desired amount of pressing force.When springs fails,high-pressure cavity and low-pressure cavity will be connected.Spring performance will directly affect the efficiency of a Wankel compressor.In this paper,we aim to introduce kinematic analysis of apex seals and force analysis of springs in a miniature Wankel compressor

Enhancing the efficacy of cytotoxic agents for cancer therapy using photochemical internalisation.

Photochemical internalisation (PCI) is a technique for improving cellular delivery of certain bioactive agents which are prone to sequestration within endolysosomes. There is a wide range of agents suitable for PCI-based delivery including toxins, oligonucleotides, genes and immunoconjugates which demonstrates the versatility of this technique. The basic mechanism of PCI involves triggering release of the agent from endolysosomes within the target cells using a photosensitiser which is selectively retained with the endolysosomal membranes. Excitation of the photosensitiser by visible light leads to disruption of the membranes via photooxidative damage thereby releasing the agent into the cytosol. This treatment enables the drugs to reach their intended subcellular target more efficiently and improves their efficacy. In this review we summarise the applications of this technique with the main emphasis placed on cancer chemotherapy

Soliton strings and interactions in mode-locked lasers

Soliton strings in mode-locked lasers are obtained using a variant of the nonlinear Schrodinger equation, appropriately modified to model power (intensity) and energy saturation. This equation goes beyond the well-known master equation often used to model these systems. It admits mode-locking and soliton strings in both the constant dispersion and dispersion-managed systems in the (net) anomalous and normal regimes; the master equation is contained as a limiting case. Analysis of soliton interactions show that soliton strings can form when pulses are a certain distance apart relative to their width. Anti-symmtetric bi-soltion states are also obtained. Initial states mode-lock to these states under evolution. In the anomalous regime individual soliton pulses are well approximated by the solutions of the unperturbed nonlinear Schrodinger equation, while in the normal regime the pulses are much wider and strongly chirped.Comment: 10 page

Henipavirus Mediated Membrane Fusion, Virus Entry and Targeted Therapeutics

The Paramyxoviridae genus Henipavirus is presently represented by the type species Hendra and Nipah viruses which are both recently emerged zoonotic viral pathogens responsible for repeated outbreaks associated with high morbidity and mortality in Australia, Southeast Asia, India and Bangladesh. These enveloped viruses bind and enter host target cells through the coordinated activities of their attachment (G) and class I fusion (F) envelope glycoproteins. The henipavirus G glycoprotein interacts with host cellular B class ephrins, triggering conformational alterations in G that lead to the activation of the F glycoprotein, which facilitates the membrane fusion process. Using the recently published structures of HeV-G and NiV-G and other paramyxovirus glycoproteins, we review the features of the henipavirus envelope glycoproteins that appear essential for mediating the viral fusion process, including receptor binding, G-F interaction, F activation, with an emphasis on G and the mutations that disrupt viral infectivity. Finally, recent candidate therapeutics for henipavirus-mediated disease are summarized in light of their ability to inhibit HeV and NiV entry by targeting their G and F glycoproteins

Vascular plant‐mediated controls on atmospheric carbon assimilation and peat carbon decomposition under climate change

Climate change can alter peatland plant community composition by promoting the growth of vascular plants. How such vegetation change affects peatland carbon dynamics remains, however, unclear. In order to assess the effect of vegetation change on carbon uptake and release, we performed a vascular plant‐removal experiment in two Sphagnum‐dominated peatlands that represent contrasting stages of natural vegetation succession along a climatic gradient. Periodic measurements of net ecosystem CO2 exchange revealed that vascular plants play a crucial role in assuring the potential for net carbon uptake, particularly with a warmer climate. The presence of vascular plants, however, also increased ecosystem respiration, and by using the seasonal variation of respired CO2 radiocarbon (bomb‐14C) signature we demonstrate an enhanced heterotrophic decomposition of peat carbon due to rhizosphere priming. The observed rhizosphere priming of peat carbon decomposition was matched by more advanced humification of dissolved organic matter, which remained apparent beyond the plant growing season. Our results underline the relevance of rhizosphere priming in peatlands, especially when assessing the future carbon sink function of peatlands undergoing a shift in vegetation community composition in association with climate change

Platelets Alter Gene Expression Profile in Human Brain Endothelial Cells in an In Vitro Model of Cerebral Malaria

Platelet adhesion to the brain microvasculature has been associated with cerebral malaria (CM) in humans, suggesting that platelets play a role in the pathogenesis of this syndrome. In vitro co-cultures have shown that platelets can act as a bridge between Plasmodium falciparum-infected red blood cells (pRBC) and human brain microvascular endothelial cells (HBEC) and potentiate HBEC apoptosis. Using cDNA microarray technology, we analyzed transcriptional changes of HBEC in response to platelets in the presence or the absence of tumor necrosis factor (TNF) and pRBC, which have been reported to alter gene expression in endothelial cells. Using a rigorous statistical approach with multiple test corrections, we showed a significant effect of platelets on gene expression in HBEC. We also detected a strong effect of TNF, whereas there was no transcriptional change induced specifically by pRBC. Nevertheless, a global ANOVA and a two-way ANOVA suggested that pRBC acted in interaction with platelets and TNF to alter gene expression in HBEC. The expression of selected genes was validated by RT-qPCR. The analysis of gene functional annotation indicated that platelets induce the expression of genes involved in inflammation and apoptosis, such as genes involved in chemokine-, TREM1-, cytokine-, IL10-, TGFβ-, death-receptor-, and apoptosis-signaling. Overall, our results support the hypothesis that platelets play a pathogenic role in CM