39 research outputs found

    Finding father, finding Mei Mei: a Chinese counsellor’s exploration on the integration of EFT and Christian prayer in trauma recovery

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    This thesis is an in-depth self-as-subject heuristic inquiry into the integration of EFT and Christian prayer in trauma recovery. It aims to support therapists who work with clients who have a personal relationship with their God, whether the therapists themselves do or not. This research is original in bringing together EFT and Christian prayer. Existing research mainly focuses on the integration of CBT or the psychodynamic tradition with Christian spirituality. This project adopts heuristic inquiry as its methodological foundation, echoing the power of experiential counselling techniques. This inquiry draws from my experience of counsellor training in the UK that exposed my emotional block to anger to myself and others. I explore how my identity as a Chinese woman encouraged this (non-)relationship to anger (or other commonly unwelcomed emotions). Both -emotion-focused therapy (EFT) procedures and Christian prayer healing contributed to a breakthrough on my work with the emotional block, which fascinated and motivated me to explore the integration of the two. I bring my own personal experience that serves the purpose of reflecting the nature of trauma therapy. At times, as in trauma recovery itself, it is sometimes messy, sometimes incoherent and fragmented and sometimes adopts a voice from a younger part of myself. By applying the integration of EFT and Christian prayer on my own therapy following an internal calling of finding father for a dissociated part of me, I have found Mei Mei (an infant part of me) and God, leading to a personal integration and development. EFT techniques are shown helpful in improving the client’s relationship with their emotions and their spirituality (relationship with God), while a relationship with God may be a pre-existing client resource and a product of therapy which continues to strengthen and consolidate the client’s recovery. I then discovered that the theme of integration applies in both my personal and professional life as a client, counsellor and researcher, whereby I have a constant need to balance ‘being and doing’, ‘relationship and technique’ and ‘deconstruct and re-construct’ in a dialectic/dialogical manner facing complex human issues. By comparing EFT and the Christian value of relationships and unconditional love to people, the thesis concludes by clarifying the potential of the integration of EFT and Christian prayer in trauma recovery

    Biological control of Fusarium crown rot of wheat with Chaetomium globosum 12XP1-2-3 and its effects on rhizosphere microorganisms

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    Chaetomium globosum is a common plant endophytic fungi that exhibits great biocontrol potential in plant disease. Fusarium crown rot (FCR) is an important disease in wheat that seriously threatens wheat production worldwide. The control effect of C. globosum against wheat FCR remains unclear. In this study, we introduced an identified C. globosum 12XP1-2-3 and tested its biological control potential against wheat FCR. The hypha and fermentation broth exhibited an antagonistic effect against Fusarium pseudograminearum. Results from indoor experiments showed that C. globosum 12XP1-2-3 might delay the onset of symptoms of brown stem base and significantly reduced the disease index (37.3%). Field trials showed that wheat seeds coated with a spore suspension of 12XP1-2-3 grew better than the control seeds, had control effects of 25.9–73.1% on FCR disease, and increased wheat yield by 3.2–11.9%. Analysis of rhizosphere microorganisms revealed that seeds coated with C. globosum (‘Cg’ treatment) had a greater effect on fungal rather than on bacterial alpha diversity and may improve the health state of rhizosphere microorganisms, as reflected by the significantly increased fungal Shannon index at Feekes 11 and the increased complexity of the bacterial co-occurrence network but decreased complexity of the fungal network. Moreover, the accumulation of beneficial bacteria such as Bacillus and Rhizobium at Feekes 3, and Sphingomonas at Feekes 7 in the ‘Cg’ treatment may be the important contributions to healthier wheat growth state, significantly reduced relative abundance of Fusarium at Feekes 11, and reduced occurrence of FCR disease. These results provide a basis for further research on the mechanism of action of C. globosum and its application in the biological control of FCR in the field

    Regulation of Respiration and Apoptosis by Cytochrome c Threonine 58 Phosphorylation

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    Cytochrome c (cytc) is a multifunctional protein, acting as an electron carrier in the electron transport chain (ETC), where it shuttles electrons from bc1 complex to cytochrome c oxidase (COX), and as a trigger of type II apoptosis when released from the mitochondria. We previously showed that cytc is regulated in a highly tissue-specific manner: Cytc isolated from heart, liver, and kidney is phosphorylated on Y97, Y48, and T28, respectively. Here, we have analyzed the effect of a new Cytc phosphorylation site, threonine 58, which we mapped in rat kidney Cytc by mass spectrometry. We generated and overexpressed wild-type, phosphomimetic T58E, and two controls, T58A and T58I cytc; the latter replacement is found in human and testis-specific Cytc. In vitro, COX activity, caspase-3 activity, and heme degradation in the presence of H2o2 were decreased with phosphomimetic Cytc compared to wild-type. Cytc-knockout cells expressing T58E or T58I Cytc showed a reduction in intact cell respiration, mitochondrial membrane potential (∆Ψm), ROS production, and apoptotic activity compared to wild-type. We propose that, under physiological conditions, Cytc is phosphorylated, which controls mitochondrial respiration and apoptosis. Under conditions of stress Cytc phosphorylations are lost leading to maximal respiration rates, ∆Ψm hyperpolarization, ROS production, and apoptosis

    Tissue‐specific regulation of cytochrome c by post‐translational modifications: respiration, the mitochondrial membrane potential, ROS, and apoptosis

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    Cytochrome c (Cytc) plays a vital role in the mitochondrial electron transport chain (ETC). In addition, it is a key regulator of apoptosis. Cytc has multiple other functions including ROS production and scavenging, cardiolipin peroxidation, and mitochondrial protein import. Cytc is tightly regulated by allosteric mechanisms, tissue‐specific isoforms, and post‐translational modifications (PTMs). Distinct residues of Cytc are modified by PTMs, primarily phosphorylations, in a highly tissue‐specific manner. These modifications downregulate mitochondrial ETC flux and adjust the mitochondrial membrane potential (ΔΨm), to minimize reactive oxygen species (ROS) production under normal conditions. In pathologic and acute stress conditions, such as ischemia–reperfusion, phosphorylations are lost, leading to maximum ETC flux, ΔΨm hyperpolarization, excessive ROS generation, and the release of Cytc. It is also the dephosphorylated form of the protein that leads to maximum caspase activation. We discuss the complex regulation of Cytc and propose that it is a central regulatory step of the mammalian ETC that can be rate limiting in normal conditions. This regulation is important because it maintains optimal intermediate ΔΨm, limiting ROS generation. We examine the role of Cytc PTMs, including phosphorylation, acetylation, methylation, nitration, nitrosylation, and sulfoxidation and consider their potential biological significance by evaluating their stoichiometry.—Kalpage, H. A., Bazylianska, V., Recanati, M. A., Fite, A., Liu, J., Wan, J., Mantena, N., Malek, M. H., Podgorski, I., Heath, E. I., Vaishnav, A., Edwards, B. F., Grossman, L. I., Sanderson, T. H., Lee, I., Hüttemann, M. Tissue‐specific regulation of cytochrome c by post‐translational modifications: respiration, the mitochondrial membrane potential, ROS, and apoptosis. FASEB J. 33, 1540–1553 (2019). www.fasebj.orgPeer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/154496/1/fsb2fj201801417r.pd

    Lysine 53 Acetylation of Cytochrome c in Prostate Cancer: Warburg Metabolism and Evasion of Apoptosis

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    Prostate cancer is the second leading cause of cancer-related death in men. Two classic cancer hallmarks are a metabolic switch from oxidative phosphorylation (OxPhos) to glycolysis, known as the Warburg effect, and resistance to cell death. Cytochrome c (Cytc) is at the intersection of both pathways, as it is essential for electron transport in mitochondrial respiration and a trigger of intrinsic apoptosis when released from the mitochondria. However, its functional role in cancer has never been studied. Our data show that Cytc is acetylated on lysine 53 in both androgen hormone-resistant and -sensitive human prostate cancer xenografts. To characterize the functional effects of K53 modification in vitro, K53 was mutated to acetylmimetic glutamine (K53Q), and to arginine (K53R) and isoleucine (K53I) as controls. Cytochrome c oxidase (COX) activity analyzed with purified Cytc variants showed reduced oxygen consumption with acetylmimetic Cytc compared to the non-acetylated Cytc (WT), supporting the Warburg effect. In contrast to WT, K53Q Cytc had significantly lower caspase-3 activity, suggesting that modification of Cytc K53 helps cancer cells evade apoptosis. Cardiolipin peroxidase activity, which is another proapoptotic function of the protein, was lower in acetylmimetic Cytc. Acetylmimetic Cytc also had a higher capacity to scavenge reactive oxygen species (ROS), another pro-survival feature. We discuss our experimental results in light of structural features of K53Q Cytc, which we crystallized at a resolution of 1.31 Å, together with molecular dynamics simulations. In conclusion, we propose that K53 acetylation of Cytc affects two hallmarks of cancer by regulating respiration and apoptosis in prostate cancer xenografts

    Towards Distributed Lexicographically Fair Resource Allocation with an Indivisible Constraint

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    In the cloud computing and big data era, data analysis jobs are usually executed over geo-distributed data centers to make use of data locality. When there are not enough resources to fully meet the demands of all the jobs, allocating resources fairly becomes critical. Meanwhile, it is worth noting that in many practical scenarios, resources waiting to be allocated are not infinitely divisible. In this paper, we focus on fair resource allocation for distributed job execution over multiple sites, where resources allocated each time have a minimum requirement. Aiming at the problem, we propose a novel scheme named Distributed Lexicographical Fairness (DLF) targeting to well specify the meaning of fairness in the new scenario considered. To well study DLF, we follow a common research approach that first analyzes its economic properties and then proposes algorithms to output concrete DLF allocations. In our study, we leverage a creative idea that transforms DLF equivalently to a special max flow problem in the integral field. The transformation facilitates our study in that by generalizing basic properties of DLF from the view of network flow, we prove that DLF satisfies Pareto efficiency, envy-freeness, strategy-proofness, relaxed sharing incentive and 12-maximin share. After that, we propose two algorithms. One is a basic algorithm that stimulates a water-filling process. However, our analysis shows that the time complexity is not strongly polynomial. Aiming at such inefficiency, we then propose a new iterative algorithm that comprehensively leverages parametric flow and push-relabel maximal flow techniques. By analyzing the steps of the iterative algorithm, we show that the time complexity is strongly polynomial

    Field Measurements of Free Ascending Behavior of Occupants along Medium-Long Stairway

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    The human behavior of walking upstairs was studied by field measurement in a 10-storey building, which simulates the greatest depth of most underground facilities. The effects of age, gender, walking distance, and fatigue on individual free ascending speed on stairs were investigated. The experimental results showed that walking distance and fatigue due to the long-distance upward walking have great impact on the upward walking and ascent speed. When climbing over 8 floors (vertical height about 30 m), the mean ascent speeds were 0.97 m/s and 0.78 m/s for young males and females, and 0.91 m/s and 0.68 m/s for middle-aged males and females, respectively. The mean ascending speed that is used to predict the evacuation time should be combined with the traveling distance or floor levels. Ascent speed models for males and females walking along a medium-long stairway were developed to describe the fatigue effect on ascending speed based on the vertical heights travelled

    iTRAQ-based high-throughput proteomics analysis reveals alterations of plasma proteins in patients infected with human bocavirus.

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    Human bocavirus (HBoV) is a member of the genus Bocavirus, family Parvoviridae, and subfamily Parvovirus and was first identified in nasopharyngeal aspirates of Swedish children with acute respiratory tract infection (ARTI) in 2005. It is the causative agent of nasopharyngeal aspirate disease and death in children. The HboV genomic structure is a linear single-stranded DNA (ssDNA). Its clinical pathogenic characteristics have been extensively studied, however, at present the molecular mechanism underlying the pathogenesis of HBoV infection is not completely clear. In this study, a total of 293 differentially expressed proteins (DEPs) between ARTI cases and healthy plasma samples were characterized using isobaric tags for relative and absolute quantitation (iTRAQ)-coupled bioinformatics analysis, among which 148 were up-regulated and 135 were down-regulated. Gene Ontology (GO) and Cluster of Orthologous Groups of proteins (COG) annotated an enrichment of DEPs in complement activation and biological processes like immunity, inflammation, signal transduction, substance synthesis, and metabolism. Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis enriched DEPs mainly in the Wnt signaling pathway (ko04310), PPAR signaling pathway (ko03320), intestinal immune network for IgA production (ko04672), complement and coagulation cascades (ko04610), Toll-like receptor signaling pathway (ko04620) and B cell receptor signaling pathway (ko04662). Further, expression levels of three candidate proteins (upregulated PPP2R1A and CUL1, and downregulated CETP) were validated using western blotting. Our investigation is the first analysis of the proteomic profile of HBoV-infected ARTI cases using the iTRAQ approach, providing a foundation for a better molecular understanding of the pathogenesis of ARTI in children

    Arsenic Activates the ER Stress-Associated Unfolded Protein Response via the Activating Transcription Factor 6 in Human Bronchial Epithelial Cells

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    Arsenic is a well-known human carcinogen associated with a number of cancers, including lung cancers. We have previously shown that long-term exposure to an environmentally relevant concentration of inorganic arsenic (As3+) leads to the malignant transformation of the BEAS2B cells, and some of the transformed cells show cancer stem-like features (CSCs) with a significant upregulation of glycolysis and downregulation of mitochondrial oxidative phosphorylation. In the present report, we investigate the short-term effect of As3+ on the endoplasmic reticulum (ER) stress response—the “unfolded protein response (UPR)” and metabolism in human bronchial epithelial cell line BEAS-2B cells. Treatment of the cells with inorganic As3+ upregulated both glycolysis and mitochondrial respiration. Analysis of ER UPR signaling pathway using a real-time human UPR array revealed that As3+ induced a significant up-regulation of some UPR genes, including ATF6, CEBPB, MAPK10, Hsp70, and UBE2G2. Additional tests confirmed that the induction of ATF6, ATF6B and UBE2G2 mRNAs and/or proteins by As3+ is dose dependent. Chromosome immunoprecipitation and global sequencing indicated a critical role of Nrf2 in mediating As3+-induced expression of these UPR genes. In summary, our data suggest that As3+ is able to regulate the ER stress response, possibly through activating the ATF6 signaling
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