Low temperature structural phase transition and incommensurate lattice modulation in the spin gap compound BaCuSi2O6

Results of high resolution x-ray diffraction experiments are presented for single crystals of the spin gap compound BaCuSi$_2$O$_6$ in the temperature range from 16 to 300 K. The data show clear evidence of a transition from the room temperature tetragonal phase into an incommensurately modulated orthorhombic structure below $\sim$100 K. This lattice modulation is characterized by a resolution limited wave vector {\bf q}$_{IC}$=(0,$\sim$0.13,0) and its 2$^{nd}$ and 3$^{rd}$ harmonics. The phase transition is first order and exhibits considerable hysteresis. This observation implies that the spin Hamiltonian representing the system is more complex than originally thought.Comment: 4 pages, 4 figure

Towards A Lightweight Incentive Scheme for Peer-to-Peer Systems

Peer-to-peer (p2p) systems rely on the contributions of peers to operate. In order to not only depend on the altruism of individual peers, a number of incentive systems have been proposed. However many of them are complex and suffer from high overhead. In this work we propose BioTrust, a lightweight incentive scheme. In contrast to other approaches, it does not require reputation histories and can operate with minimal overhead in terms of bandwidth, infrastructure, memory and computation. BioTrust is based on observations of cooperation as observed in biological systems, which show that individuals try to ally themselves with others that can best increase their own standing. Such observations are prevalent in evolutionary systems where individuals must weigh off their own individual needs against the need for cooperation to survive. Using these models, BioTrust has been developed to extract and modify some of the most useful properties of biological systems to work effectively in a p2p environment. It is shown through simulation that this scheme encourages honest peers, which leads to a close to optimal behavior in the system context as well as for single peers

Phenotypic analysis of IL-9/IL-9R and KIF21B in multiple sclerosis and the role of HIF-1 in its animal model

Multiple sclerosis (MS) is the predominant cause of persistent, non-traumatic neurological disability in young adults of the western world. The disease is defined by inflammation and neurodegeneration, however, the precise mechanisms underlying immunopathogenesis and neurodegeneration remain to be fully comprehended. Pathological mechanisms implicated in MS include, for example: (i) hypoxia-like tissue injury, (ii) impaired neuronal transport, and (iii) cytokine-mediated immunopathogenesis and these were therefore investigated in this thesis. Hypoxia-like tissue injury has been associated with MS, and the action of hypoxia inducible factor (HIF)-1 has been suggested to protect against such injury. To investigate a potential beneficial effect of the HIF-1 pathway in MS, HIF-1 was pharmacologically stabilised in a murine model of MS. However, no effect on disease development or progression was observed, suggesting that a general induction of H1F 1-dependent pathways may not be a viable therapeutic avenue for MS A molecular motor protein termed kinesin family member 21 B (K1F21 B) that has a suggested function in neuronal transport has recently been implicated in MS as a potential disease-associated candidate gene. A histopathological analysis demonstrated the expression of KIF21B in the neuronal compartment of human post mortem brain tissue. Intriguingly, however, differential expression of KIF21B was only detected in the immunological compartment and was associated with increasing demyelinating lesion activity. This observation is striking as it implies an immunological rather than neuronal role of K1F21 B in MS. Whilst interleukin (I L)-9 and its receptor (IL-9R) have been implicated in a murine model of MS, this cytokine pathway has not been previously characterised in the human disease. Histopathological examination demonstrated a low frequency of lL-9/1L -9 1~ expressing immune cells in MS lesions, suggesting a minor role of the immunological arm of this pathway in the central nervous system. However, in the neuronal compartment there was a notable inverse correlation between IL-9R levels and white matter lesion activity that implicates IL-9R signalling in the modulation of neurona1 responses in MS pathology. Collectively this work provides new insight into several different aspects of MS pathogenesis.EThOS - Electronic Theses Online ServiceGBUnited Kingdo

Changes of the balancing between anode and cathode due to fatigue in commercial lithium-ion cells

The electrode balancing defines the state of charge (SoC) of a lithium-ion cell and is a crucial point considering lifetime and safe operation. The electrode balancing varies during fatigue which results in changes of the individual electrode potentials for fixed (dis-)charge voltages of the full-cell. Therefore the materials are cycled closer or beyond their electrochemical (meta-)stability window. This leads to accelerated degradation reactions or even to safety problems. The origin of the changes in the cell balancing is the limited amount of mobile lithium, which decreases during cycling due to the loss of lithiated active material a), the reduction of accessible lattice sites in the active materials b) and the loss of active lithium outside the electrodes c). In most of the commercial cells a) and b) can be attributed to the cathode, c) occurs due to reactions on the anode surface. Changes in the electrode balancing of three differently fatigued 7 Ah lithium-ion cells are investigated by electrochemical cycling of full- and half-cells, assembled from cell components of the fatigued 7 Ah cells. Based on these results the observed performance drop is assigned to a), b) or c) mentioned above and the capacity losses are quantified

STAT signaling in polycystic kidney disease

The most common form of polycystic kidney disease (PKD) in humans is caused by mutations in the PKD1 gene coding for polycystin1 (PC1). Among the many identified or proposed functions of PC1 is its ability to regulate the activity of transcription factors of the STAT family. Most STAT proteins that have been investigated were found to be aberrantly activated in kidneys in PKD, and some have been shown to be drivers of disease progression. In this review, we focus on the role of signal transducer and activator of transcription (STAT) signaling pathways in various renal cell types in healthy kidneys as compared to polycystic kidneys, on the mechanisms of STAT regulation by PC1 and other factors, and on the possibility to target STAT signaling for PKD therapy

Structure and dynamics of UBA5-UFM1 complex formation showing new insights in the UBA5 activation mechanism

Ubiquitin fold modifier 1 (UFM1) is an ubiquitin-like protein (Ubl) involved especially in endoplasmic stress response. Activation occurs via a three-step mechanism like other Ubls. Data obtained reveal that UFM1 regulates the oligomeric state of ubiquitin activating enzyme 5 (UBA5) to initiate the activation step. Mixtures of homodimers and heterotrimers are observed in solution at the equilibrium state, demonstrating that the UBA5-UFM1 complex undergoes several concentration dependent oligomeric translational states to form a final functional complex. The oligomerization state of unbound UBA5 is also concentration dependent and shifts from the monomeric to the dimeric state. Data describing different oligomeric states are complemented with binding studies that reveal a negative cooperativity for the complex formation and thereby provide more detailed insights into the complex formation mechanism