9,170 research outputs found
Thermodynamic analysis of an adsorption-based desalination cycle
No full textJun W. Wu, Mark J. Biggs, Eric J. H
C/EBPalpha downregualtes c-jun expression
No full textThe transcription factor C/EBPa is crucial for the differentiation of granulocytes. Conditional expression of C/EBPa triggers neutrophilic differentiation and C/EBPa can block TPA induced monocytic differentiation of bipotential myeloid cells. In C/EBPa knockout mice, no mature granulocytes are present. A dramatic increase of c-jun mRNA in C/EBPa knockout mice fetal liver was observed. c-jun, a component of the AP-1 transcription factor complex and a co-activator of the transcription factor PU.1, is important for monocytic differentiation. Here we report that C/EBPa downregulates c-jun expression to drive granulocytic differentiation. Ectopic increase of C/EBPa expression decreases c-jun mRNA level, and the human c-jun promoter activity is downregulated 8 fold in presence of C/EBPa. C/EBPa and c-jun interact through their leucine zipper domains and this interaction prevents c-jun from binding to DNA. This results in downregulation of c-jun’s capacity to autoregulate its own promoter through the proximal AP-1 site. Overexpression of c-jun prevents C/EBPa induced granulocytic differentiation. c-jun expression was higher in AML M2 patients with dominant negative C/EBPa mutations in comparison to AML M2 patients without C/EBPa mutations. Thus, we propose a model in which C/EBPa needs to downregulate c-jun expression and transactivation capacity for promoting granulocytic differentiation.Der Transkriptionsfaktor C/EBPa ist essentiell für die Differenzierung von Granulozyten. Die konditionelle Expression von C/EBPa induziert die neutrophile Differenzierung. Überdies kann C/EBPa die TPA-induzierte Differenzierung von myeloiden Vorläuferzellen zu Monozyten blockieren. In C/EBPa knockout Mäusen gibt es keine reifen Granulozyten. In der fötalen Leber von C/EBPa knockout Mäusen konnte eine stark erhöhte Expression der c-jun mRNA beobachtet werden. c-jun ist eine Komponente des AP-1 Transkriptionsfaktorkomplexes, ein Koaktivator des Transkriptionsfaktors PU.1 und ist wichtig für die Differenzierung von Monozyten. In dieser Arbeit zeigen wir, dass C/EBPa die c-jun Expression herunterreguliert und somit die Differenzierung von Granulozyten induziert. Die Überexpression von C/EBPa reduzierte die c-jun mRNA Menge und die Aktivität des humanen c-jun Promotors war in der Gegenwart von C/EBPa 8-fach herunterreguliert. C/EBPa und c-jun interagieren über ihre Leucin-Zipper Domänen und diese Interaktion verhindert die DNA-Bindung von c-jun. Dies resultiert in einer verminderten Kapazität von c-jun, den eigenen Promotor über die proximale AP-1 Stelle zu regulieren. Die Überexpression von c-jun blockiert die durch C/EBPa induzierte granulozytäre Differenzierung. Die c-jun Expression war in AML-M2 Patienten mit dominant-negativen Mutationen in C/EBPa im Vergleich zu AML-M2 Patienten ohne Mutationen in C/EBPa erhöht. Aufgrund dieser Daten schlagen wir ein Modell vor, in dem C/EBPa die Expression und Transaktivierungskapazität von c-jun herunterregulieren muß, um die granulozytäre Differenzierung zu induzieren
Separation principle for networked control systems with multiple-packet transmission
No full textThe authors investigate a class of observer-based discrete-time networked control systems (NCSs) with multiple-packet transmission where random packet dropouts occur independently in both the sensor-to-controller (S/C) and controller-to-actuator (C/A) channels. The authors first propose and prove the separation principle for the NCSs where packet dropouts in the C/A and S/C channels are governed by two independent Markov chains, respectively. Secondly, the authors derive a sufficient condition, in terms of linear matrix inequalities (LMIs), for stabilisation control of the Markov chain-driven NCSs. The authors also derive the necessary and sufficient condition for stabilisation control of the memoryless process-driven NCSs as a special case. A numerical example is provided to illustrate the effectiveness of our method
Robust H∞ control of networked control systems with access constraints and packet dropouts
No full textWe consider a class of networked control systems (NCSs) where the plant has time-varying norm-bounded parameter uncertainties, the network only provides a limited number of simultaneous accesses for the sensors and actuators, and the packet dropouts occur randomly in the network. For this class of NCSs with uncertainties and access constraints as well as packet dropouts, we derive sufficient conditions in the form of linear matrix inequalities that guarantee robust stochastic stabilisation and synthesis of H∞ controller. An example is provided to illustrate our proposed method
Zhong zi xing de ji xing w-mo zhen dang
No full textWu Jun = 中子星的極性w-模振盪 / 吳俊.Thesis (M.Phil.)--Chinese University of Hong Kong, 2005.Includes bibliographical references (leaves 100-102).Text in English; abstracts in English and Chinese.Wu Jun = Zhong zi xing de ji xing w-mo zhen dang / Wu Jun.Abstract --- p.iAcknowledgement --- p.iiiChapter 1 --- Introduction --- p.1Chapter 1.1 --- Background introduction and historical review --- p.1Chapter 1.2 --- Outline of the thesis --- p.3Chapter 1.3 --- Notations and conventions --- p.4Chapter 2 --- Equilibrium and oscillations of Relativistic stars --- p.5Chapter 2.1 --- Relativistic stars --- p.5Chapter 2.1.1 --- Equilibrium configuration --- p.6Chapter 2.1.2 --- Equation of state --- p.7Chapter 2.2 --- Oscillations of relativistic stars --- p.9Chapter 2.2.1 --- Families of fluid modes --- p.10Chapter 2.2.2 --- Families of spacetime modes (w-mode) --- p.11Chapter 3 --- Polar oscillations of neutron stars --- p.14Chapter 3.1 --- Axial oscillations of neutron stars --- p.14Chapter 3.2 --- LD formulation --- p.16Chapter 3.2.1 --- Equations inside star --- p.17Chapter 3.2.2 --- Boundary conditions at r = 0 and r = R --- p.19Chapter 3.2.3 --- Perturbations outside star --- p.21Chapter 3.3 --- AAKS formulation --- p.22Chapter 3.3.1 --- Equations inside the star --- p.23Chapter 3.3.2 --- Behavior at the center and the stellar surface --- p.25Chapter 3.3.3 --- Evolution outside star --- p.28Chapter 3.3.4 --- Connection formula --- p.29Chapter 4 --- QNMs of polar oscillations --- p.31Chapter 4.1 --- Solution outside star --- p.31Chapter 4.2 --- LD approach --- p.32Chapter 4.3 --- Hamiltonian constraint --- p.33Chapter 4.4 --- Boundary conditions a.t r = R --- p.37Chapter 4.5 --- Direct integration scheme (DIS) --- p.42Chapter 4.6 --- Two-way integration scheme (TIS) --- p.43Chapter 4.7 --- Connect the interior and exterior solutions --- p.45Chapter 4.8 --- Numerical results --- p.46Chapter 5 --- Polar oscillations without fluid motions --- p.50Chapter 5.1 --- Zero pressure variation approximation (ZPVA) --- p.51Chapter 5.1.1 --- Evolution formulas --- p.51Chapter 5.1.2 --- Boundary conditions --- p.53Chapter 5.1.3 --- Approximate QNMs --- p.55Chapter 5.2 --- Zero density variation approximation (ZDVA) --- p.55Chapter 5.2.1 --- Single equation formulas --- p.58Chapter 5.2.2 --- Numerical results --- p.61Chapter 5.2.3 --- Summary --- p.62Chapter 5.3 --- Application of ZDVA --- p.65Chapter 5.3.1 --- Relation between axial and polar w-modes --- p.65Chapter 5.3.2 --- Analysis --- p.66Chapter 6 --- Universal behavior of polar QNMs --- p.69Chapter 6.1 --- Universal behavior of polar w-modes --- p.70Chapter 6.2 --- Ordinary CQM of neutron stars --- p.71Chapter 6.2.1 --- TOV parameters of a CQM star --- p.71Chapter 6.2.2 --- Stability problem of CQM --- p.73Chapter 6.2.3 --- EOS near the surface --- p.75Chapter 6.3 --- Scaling behavior of polar oscillations --- p.78Chapter 6.3.1 --- Scaling behavior of fluid motions --- p.79Chapter 6.3.2 --- Scaled wave equations --- p.80Chapter 6.4 --- Scaled Cubic-Quintic Model (SCQM) --- p.82Chapter 7 --- Conclusion --- p.85Chapter 7.1 --- Summary of Our Work --- p.85Chapter 7.2 --- Outlook --- p.86Chapter A --- Expansion of Hamiltonian constraint around the center --- p.88Chapter B --- Factorization integration scheme (FIS) --- p.92Chapter C --- Equivalence of two definitions of the Zerilli function --- p.9
Crosstalk between c-Jun and TAp73alpha/beta contributes to the apoptosis–survival balance
No full textThe p53-family member p73 plays a role in various cellular signaling pathways during development and growth control and it can have tumor suppressor properties. Several isoforms of p73 exist with considerable differences in their function. Whereas the functions of the N-terminal isoforms (TA and delta Np73) and their opposing pro- and antiapoptotic roles have become evident, the functional differences of the distinct C-terminal splice forms of TAp73 have remained unclear. Here, we characterized the global genomic binding sites for TAp73alpha and TAp73beta by chromatin immunoprecipitation sequencing as well as the transcriptional responses by performing RNA sequencing. We identified a specific p73 consensus binding motif and found a strong enrichment of AP1 motifs in close proximity to binding sites for TAp73alpha. These AP1 motif-containing target genes are selectively upregulated by TAp73alpha, while their mRNA expression is repressed upon TAp73beta induction. We show that their expression is dependent on endogenous c-Jun and that recruitment of c-Jun to the respective AP1 sites was impaired upon TAp73beta expression, in part due to downregulation of c-Jun. Several of these AP1-site containing TAp73alpha-induced genes impinge on apoptosis induction, suggesting an underlying molecular mechanism for the observed functional differences between TAp73alpha and TAp73beta
Robust control for discrete-time networked control systems
No full textThis paper considers analysis and synthesis of discrete-time networked control systems (NCSs), where the plant has additive uncertainty and the controller is updated with the sensor information at stochastic time intervals. It is shown that the problem is linked to robust control of linear discrete-time stochastic systems and a new small gain theorem is established. Based on this result, sufficient conditions are given for ensuring mean square stability of the NCS, and the genetic algorithm is utilised to design the controller of the NCS based on a linear matrix inequality technique
Efficient prediction method for broadband acoustic mode radiation from engine bypass ducts
No full textHigh levels of broadband noise produced by modern high-bypass turbine engines have a significant impact on the environment. High performance computational numerical methods are now taking an active role in this research area. The research presented in this thesis explores a method for efficient prediction of broadband aeroacoustic radiation from a turbofan engine bypass duct and the effect of the multi-mode propagation in the near-field of an engine bypass duct with bifurcations installed on. An accurate and high-order Computational Aeroacoustics (CAA) numerical scheme is used in two and-half and three dimensional linearised Euler equations to determine the results. For far-field predictions, the Ffowcs Williams- Hawkings (FW-H) method and the Acoustic Intensity Based Method (AIBM) could be used to solve the single mode problem. However, the current FW-H method can not be used for multi-mode problems due to its required demand for computational resources. AIBM is an efficient tool to predict the pressure in far-field based on the near-field solution calculated by CAA, and has a potential for multi-mode prediction in the far-field. The performances of the prediction of the radiation of bypass duct acoustics with mean flow have been analysed, with particular attention to the ducts with bifurcations. For the single mode case of the duct acoustics, the AIBM has been implemented and compared against CAA results in the nearfield. Comparison between AIBM and FW-H directivity pattern in the far-field region show good agreement. The clean duct cases for multi-mode are solved with the linearised Euler equations (LEE) in two-and-half dimensions and the results are analysed. For multi-frequency cases, the SPL directivity contour almost matches the pattern obtained by summing the results computed by single frequencies. Lower radial modes contribute more to the overall SPL value than higher ones. For the circumferential modes, lower ones are more likely to cut-on to more discrete frequencies. Finally, the three dimensional solver is used to determine the near-field multi-mode radiation from a generic engine bypass with bifurcations. The bifurcations can cause the acoustic pressure waves to be redirected. Interference between the diffracted modes increased the acoustic pressures. Results show that lower radial modes are smaller in amplitude, and are more likely to cut-on when the radial modes are higher. More complex patterns have formed, because of the bifurcation interference, compared to single mode cases. For different circumferential mode cases, the radiation peak angle increases as the circumferential mode increases
Suppression of cell cycle progression by Jun dimerization protein (JDP2) involves down-regulation of cyclin A2
No full textWe report here a novel role for Jun dimerization protein-2 (JDP2) as a regulator of the progression of normal cells through the cell cycle. To determine the role of JDP2 in vivo, we generated Jdp2 knock-out (Jdp2KO) mice by targeting exon 1 to disrupt the site of initiation of transcription. The healing of wounded skin of Jdp2KO mice proceeded more rapidly than that of control mice and more proliferating cells were found at wound margins. Fibroblasts derived from embryos of Jdp2KO mice proliferated more rapidly and formed more colonies than wild-type fibroblasts. JDP2 was recruited to the promoter of the gene for cyclin A2 (ccna2) at a previously unidentified AP-1 site. Cells lacking Jdp2 had elevated levels of cyclin A2 mRNA. Moreover, reintroduction of JDP2 resulted in repression of transcription of ccna2 and of cell cycle progression. Thus, transcription of the gene for cyclin A2 appears to be a direct target of JDP2 in the suppression of cell proliferation
Transforming growth factor beta (TGF beta) mediates schwann cell death in vitro and in vivo: Examination of c-jun activation, interactions with survival signals, and the relationship of TGF beta-mediated death to schwann cell differentiation
No full textIn some situations, cell death in the nervous system is controlled by an interplay between survival factors and negative survival signals that actively induce apoptosis. The present work indicates that the survival of Schwann cells is regulated by such a dual mechanism involving the negative survival signal transforming growth factor beta (TGF beta), a family of growth factors that is present in the Schwann cells themselves. We analyze the interactions between this putative autocrine death signal and previously defined paracrine and autocrine survival signals and show that expression of a dominant negative c-Jun inhibits TGF beta -induced apoptosis. This and other findings pinpoint activation of c-Jun as a key downstream event in TGF beta -induced Schwann cell death. The ability of TGF beta to kill Schwann cells, like normal Schwann cell death in vivo, is under a strong developmental regulation, and we show that the decreasing ability of TGF beta to kill older cells is attributable to a decreasing ability of TGF beta to phosphorylate c-Jun in more differentiated cells
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