Complexing Behaviour of 2-Thioorotic Acid: Complexes of Co(II), Fe(II), Rh(III), Pd(IV) & Pt(IV)

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Schwinger-Dyson operator of Yang-Mills matrix models with ghosts and derivations of the graded shuffle algebra

We consider large-N multi-matrix models whose action closely mimics that of Yang-Mills theory, including gauge-fixing and ghost terms. We show that the factorized Schwinger-Dyson loop equations, expressed in terms of the generating series of gluon and ghost correlations G(xi), are quadratic equations S^i G = G xi^i G in concatenation of correlations. The Schwinger-Dyson operator S^i is built from the left annihilation operator, which does not satisfy the Leibnitz rule with respect to concatenation. So the loop equations are not differential equations. We show that left annihilation is a derivation of the graded shuffle product of gluon and ghost correlations. The shuffle product is the point-wise product of Wilson loops, expressed in terms of correlations. So in the limit where concatenation is approximated by shuffle products, the loop equations become differential equations. Remarkably, the Schwinger-Dyson operator as a whole is also a derivation of the graded shuffle product. This allows us to turn the loop equations into linear equations for the shuffle reciprocal, which might serve as a starting point for an approximation scheme.Comment: 13 pages, added discussion & references, title changed, minor corrections, published versio

Sumoylation is tumor-suppressive and confers proliferative quiescence to hematopoietic progenitors in Drosophila melanogaster larvae

Summary How cell-intrinsic regulation of the cell cycle and the extrinsic influence of the niche converge to provide proliferative quiescence, safeguard tissue integrity, and provide avenues to stop stem cells from giving rise to tumors is a major challenge in gene therapy and tissue engineering. We explore this question in sumoylation-deficient mutants of Drosophila. In wild type third instar larval lymph glands, a group of hematopoietic stem/progenitor cells acquires quiescence; a multicellular niche supports their undifferentiated state. However, how proliferative quiescence is instilled in this population is not understood. We show that Ubc9 protein is nuclear in this population. Loss of the SUMO-activating E1 enzyme, Aos1/Uba2, the conjugating E2 enzyme, Ubc9, or the E3 SUMO ligase, PIAS, results in a failure of progenitors to quiesce; progenitors become hyperplastic, misdifferentiate, and develop into microtumors that eventually detach from the dorsal vessel. Significantly, dysplasia and lethality of Ubc9 mutants are rescued when Ubc9wt is provided specifically in the progenitor populations, but not when it is provided in the niche or in the differentiated cortex. While normal progenitors express high levels of the Drosophila cyclin-dependent kinase inhibitor p21 homolog, Dacapo, the corresponding overgrown mutant population exhibits a marked reduction in Dacapo. Forced expression of either Dacapo or human p21 in progenitors shrinks this population. The selective expression of either protein in mutant progenitor cells, but not in other hematopoietic populations, limits overgrowth, blocks tumorogenesis, and restores organ integrity. We discuss an essential and complex role for sumoylation in preserving the hematopoietic progenitor states for stress response and in the context of normal development of the fly

Possible large-N fixed-points and naturalness for O(N) scalar fields

We try to use scale-invariance and the large-N limit to find a non-trivial 4d O(N) scalar field model with controlled UV behavior and naturally light scalar excitations. The principle is to fix interactions by requiring the effective action for space-time dependent background fields to be finite and scale-invariant when regulators are removed. We find a line of non-trivial UV fixed-points in the large-N limit, parameterized by a dimensionless coupling. They reduce to classical la phi^4 theory when hbar -> 0. For hbar non-zero, neither action nor measure is scale-invariant, but the effective action is. Scale invariance makes it natural to set a mass deformation to zero. The model has phases where O(N) invariance is unbroken or spontaneously broken. Masses of the lightest excitations above the unbroken vacuum are found. We derive a non-linear equation for oscillations about the broken vacuum. The interaction potential is shown to have a locality property at large-N. In 3d, our construction reduces to the line of large-N fixed-points in |phi|^6 theory.Comment: 23 page

Transport methods and interactions for space radiations

A review of the program in space radiation protection at the Langley Research Center is given. The relevant Boltzmann equations are given with a discussion of approximation procedures for space applications. The interaction coefficients are related to solution of the many-body Schroedinger equation with nuclear and electromagnetic forces. Various solution techniques are discussed to obtain relevant interaction cross sections with extensive comparison with experiments. Solution techniques for the Boltzmann equations are discussed in detail. Transport computer code validation is discussed through analytical benchmarking, comparison with other codes, comparison with laboratory experiments and measurements in space. Applications to lunar and Mars missions are discussed

Identification of Movement Strategies during the Sit-to-Walk Movement in Patients with Knee Osteoarthritis

Patients with osteoarthritis (OA) of the knee commonly alter their movement to compensate for deficiencies. This study presents a new numerical procedure for classifying sit-to-walk (STW) movement strategies. Ten control and twelve OA participants performed the STW task in a motion capture laboratory. A full body biomechanical model was used. Participants were instructed to sit in a comfortable self-selected position on a stool height adjusted to 100% of their knee height and then stand and pick up an object from a table in front of them. Three matrices were constructed defining the progression of the torso, feet and hands in the sagittal plane along with a fourth expressing the location of the hands relative to the knees. Hierarchical clustering (HC) was used to identify different strategies. Trials were also classified as to whether the left (L) and right (R) extremities used a matching strategy (bilateral) or not (asymmetrical). Fisher’s exact test was used to compare this between groups. Clustering of the torso matrix dichotomised the trials in two major clusters; subjects leaning forward (LF) or not. The feet and hands matrices revealed sliding the foot backward (FB) and moving an arm forward (AF) strategies respectively. Trials not belonging in the AF cluster were submitted to the last HC of the fourth matrix exposing three additional strategies, the arm pushing through chair (PC), arm pushing through knee (PK) and arm not used (NA). The control participants used the LF+FBR+PK combination most frequently whereas the OA participants used the AFR+PCL. OA patients used significantly more asymmetrical arm strategies, p=0.034. The results demonstrated that control and OA participants favour different STW strategies. The OA patients asymmetrical arm behaviour possibly indicates compensating for weakness of the affected leg. These strategy definitions may be useful to assess post-operative outcomes and rehabilitation progress

Translational control of the SigR-directed oxidative stress response in streptomyces via IF3-mediated repression of a noncanonical GTC start codon

The major oxidative stress response in Streptomyces is controlled by the sigma factor SigR and its cognate antisigma factor RsrA, and SigR activity is tightly controlled through multiple mechanisms at both the transcriptional and posttranslational levels. Here we show that sigR has a highly unusual GTC start codon and that this leads to another level of SigR regulation, in which SigR translation is repressed by translation initiation factor 3 (IF3). Changing the GTC to a canonical start codon causes SigR to be overproduced relative to RsrA, resulting in unregulated and constitutive expression of the SigR regulon. Similarly, introducing IF3* mutations that impair its ability to repress SigR translation has the same effect. Thus, the noncanonical GTC sigR start codon and its repression by IF3 are critical for the correct and proper functioning of the oxidative stress regulatory system. sigR and rsrA are cotranscribed and translationally coupled, and it had therefore been assumed that SigR and RsrA are produced in stoichiometric amounts. Here we show that RsrA can be transcribed and translated independently of SigR, present evidence that RsrA is normally produced in excess of SigR, and describe the factors that determine SigR-RsrA stoichiometry.IMPORTANCE In all sigma factor-antisigma factor regulatory switches, the relative abundance of the two proteins is critical to the proper functioning of the system. Many sigma-antisigma operons are cotranscribed and translationally coupled, leading to a generic assumption that the sigma and antisigma factors are produced in a fixed 1:1 ratio. In the case of sigR-rsrA, we show instead that the antisigma factor is produced in excess over the sigma factor, providing a buffer to prevent spurious release of sigma activity. This excess arises in part because sigR has an extremely rare noncanonical GTC start codon, and as a result, SigR translation initiation is repressed by IF3. This finding highlights the potential significance of noncanonical start codons, very few of which have been characterized experimentally. It also emphasizes the limitations of predicting start codons using bioinformatic approaches, which rely heavily on the assumption that ATG, GTG, and TTG are the only permissible start codons