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Case Study Of the Signature Project – An Australian–Us Knowledge Translation Project
Published in Gill Harvey, Alison Kitson, Implementing Evidence-Based Practice In Healthcare, 2015
Alison Kitson, Rick Wiechula, Tiff Conroy, Nancy Whitaker, Cheryl Holly, Susan Salmond
Although the terminology relating to facilitation and KT may have been unfamiliar to some, the skills and tools to achieve this are often linked to other experiences. The IFs in site B, for example, had extensive experience in evidence-based practice and they drew on this to shape the beginning of the project: Lead people through evidence; let them look at the articles, doing searches, and guiding them. It involves IT, policy change, education, and communication. We both have links to several different universities, which helps build sustainability and capacity. Students from every level, from associate degrees to PhDs.(IF1&2 site B)
Modeling the therapy system of noninvasive pressure support ventilation with the respiratory patient in COPD and ARDS
Published in Computer Methods in Biomechanics and Biomedical Engineering, 2023
Yueyang Yuan, Lixin Xie, Wei Liu, Zheng Dai
According to the mathematical model of NPSV therapy system, a MATLAB-based simulation was designed as illustrated in Figure 4. In the simulation, the module program of “if1” was designed to carry out the function of Equation (1). In this module program of “if1”, when Qa > IPAPtrig, the respirator will be trigged to output the pressure of IPAP (i.e. Pa = IPAP). When Qa < EPAPtrig, the respirator will be trigged to output the pressure of IPAP (i.e. Pa = EPAP). The module program of “if2” was designed to carry out the function of Equation (2). “The block of RLeak” was designed to conduct out the function of Equation (3) in which a ≈ 0.2 and b ≈ 0.65 were calibrated with an oral-nasal mask Bestfit2 (Curative Medical Inc., Santa Clara, CA).
Mitoquinone restores platelet production in irradiation-induced thrombocytopenia
Published in Platelets, 2015
Haley Ramsey, Qi Zhang, Mei X. Wu
IEX-1 expression is found throughout the body, varying in levels in different tissues and organs and can be strongly upregulated in response to stressors such as irradiation, viral infections, growth factors, and steroid hormones [8]. Its main functions are not only regulation of reactive oxygen species (ROS), but also control of the fate of stressed cells [9–11]. Its anti-apoptotic quality lies, at least in part, on maintenance of ROS homeostasis at mitochondria [10, 12]. While a low-level of ROS serve as secondary messengers in signaling cascades regulating cell proliferation and homeostasis, significant increases of ROS enhances susceptibility of cells to apoptosis. We have shown that IEX-1 targets F1F0-ATPase inhibitor (IF1) for degradation and IF1 degradation prevents a rise of ROS triggered by various apoptotic stimuli thereby protecting cells from undergoing apoptosis [10]. In contrast, loss of IEX-1 modestly elevates ROS formation, rendering some cells susceptible to apoptosis, but altering cell-signaling, differentiation, and maturation in others, depending on the level of ROS production in individual cells [4, 13].
scRNA-seq reveals ATPIF1 activity in control of T cell antitumor activity
Published in OncoImmunology, 2022
Genshen Zhong, Qi Wang, Ying Wang, Ying Guo, Meiqi Xu, Yaya Guan, Xiaoying Zhang, Minna Wu, Zhishan Xu, Weidong Zhao, Hongkai Lian, Hui Wang, Jianping Ye
Above data demonstrated that the CD8+ T cells exhibited a decreased antitumor activity in the KO mice. Mitochondrial activities were examined in the cells to understand mechanism of the decrease. F1Fo-ATP synthase makes as well as hydrolyzes ATP, and both activities rise in the absence of ATPIF1.24 Such alterations were not verified in T cells before this study. Mitochondrial potential (Δψm) and intracellular ATP content were examined to address the issue. CD8+ T cells were isolated from the spleen and used in the following experiments. Δψm was determined in the intact cells using JC-1, a lipophilic and cationic dye for detection of mitochondria membrane potential.25 The KO cells exhibited normal Δψm in the resting condition as shown by the JC-1 red/green ratio (Figure 2a). In the activation condition, the KO cells had a higher Δψm following a sharp Δψm reduction in the WT cells. The KO cell had more intracellular ATP content in the resting and activated conditions (Figure 2b), supporting an increase in ATP synthesis. Additionally, IF1 plays a role in the modulation of mitochondrial cristae.12,26 Mitochondrial mass was determined using MitoTracker staining. The KO cells had a lower mitochondrial mass in the resting condition as indicated by MFI (Figure 2c). However, the difference disappeared after cell activation as the WT cells displayed a remarkable mass reduction in response to the activation (Figure 2c). ROS, determined with the fluorescent probe DCFH-DA, revealed that the KO cells had a normal ROS level in the resting condition, but less ROS in the activated status (Figure 2d). Manipulation of ROS with N acetylcysteine (NAC) in vivo could not remove the difference in tumor growth between the KO and WT mice (Fig. S2), suggesting that ROS may not be responsible for the difference in tumor immunity. IFN-γ secretion and cell proliferation were examined to understand the impact of mitochondrial alteration. Following activation, the KO cells produced less IFN-γ as determined by the flow cytometry (Figure 2e, p < .0001). The proliferation activity was decreased as well in the CFSE-labeled experiment (Figure 2f). These data demonstrate that ATPIF1 deficiency reprogrammed the energy metabolism in CD8+ T cells for a reduced antitumor efficacy.