Contractions of sigma models and integration of massive modes

We show how the integration of massive modes after a spontaneous symmetry breaking in a sigma model can often be interpreted as a contraction, induced by a group contraction, of the target space of the sigma model.Comment: 9 pages. Prepared for the porceedings of the 4-th International Symposium Quantum Theory and Symmetries. Varna, Bulgaria, 15-21 August 200

Special geometry for arbitrary signatures

In this paper we generalize special geometry to arbitrary signatures in target space. We formulate the definitions in a precise mathematical setting and give a translation to the coordinate formalism used in physics. For the projective case, we first discuss in detail projective Kaehler manifolds, appearing in N=1 supergravity. We develop a new point of view based on the intrinsic construction of the line bundle. The topological properties are then derived and the Levi-Civita connection in the projective manifold is obtained as a particular projection of a Levi-Civita connection in a `mother' manifold with one extra complex dimension. The origin of this approach is in the superconformal formalism of physics, which is also explained in detail. Finally, we specialize these results to projective special Kaehler manifolds and provide explicit examples with different choices of signature.Comment: LaTeX, 83 pages; v2: typos corrected, version to be published in Handbook of pseudo-Riemannian Geometry and Supersymmetry, IRMA Lectures in Mathematics and Theoretical Physic

Field induced magnetic transition and metastability in Co substituted Mn2SbMn_{2}Sb

A detailed investigation of first order ferrimagnetic (FRI) to antiferromagnetic (AFM) transition in Co (15%) doped $Mn_2Sb$ is carried out. These measurements demonstrate anomalous thermomagnetic irreversibility and glass-like frozen FRI phase at low temperatures. The irreversibility arising between the supercooling and superheating spinodals is distinguised in an ingenious way from the irreversibility arising due to kinetic arrest. Field annealing measurements shows reentrant FRI-AFM-FRI transition with increasing temperature. These measurements also show that kinetic arrest band and supercooling band are anitcorrelated i.e regions which are kinetically arrested at higher temperature have lower supercooling temperature and vice versa.Comment: 10 pages, 8 figure

The Pit-1/Pou1f1 transcription factor regulates and correlates with prolactin expression in human breast cell lines and tumors

The transcription factor Pit-1/Pou1f1 regulates GH and prolactin (PRL) secretion in the pituitary gland. Pit-1 expression and GH regulation by Pit-1 have also been demonstrated in mammary gland. However, no data are available on the role of Pit-1 on breast PRL. To evaluate this role, several human breast cancer cell lines were transfected with either the Pit-1 expression vector or a Pit-1 small interference RNA construct, followed by PRL mRNA and protein evaluation. In addition, transient transfection of MCF-7 cells by a reporter construct containing the proximal PRL promoter, and ChIP assays were performed. Our data indicate that Pit-1 regulates mammary PRL at transcriptional level by binding to the proximal PRL promoter. We also found that Pit-1 raises cyclin D1 expression before increasing PRL levels, suggesting a PRL-independent effect of Pit-1 on cell proliferation. By using immunohistochemistry, we found a significant correlation between Pit-1 and PRL expression in 94 human breast invasive ductal carcinomas. Considering the possible role of PRL in breast cancer disorders, the function of Pit-1 in breast should be the focus of further research

A global Carleman estimate in a transmission wave equation and application to a one-measurement inverse problem

We consider a transmission wave equation in two embedded domains in $R^2$, where the speed is $a1 > 0$ in the inner domain and $a2 > 0$ in the outer domain. We prove a global Carleman inequality for this problem under the hypothesis that the inner domain is strictly convex and $a1 > a2$ . As a consequence of this inequality, uniqueness and Lip- schitz stability are obtained for the inverse problem of retrieving a stationary potential for the wave equation with Dirichlet data and discontinuous principal coefficient from a single time-dependent Neumann boundary measurement

Networked buffering: a basic mechanism for distributed robustness in complex adaptive systems

A generic mechanism - networked buffering - is proposed for the generation of robust traits in complex systems. It requires two basic conditions to be satisfied: 1) agents are versatile enough to perform more than one single functional role within a system and 2) agents are degenerate, i.e. there exists partial overlap in the functional capabilities of agents. Given these prerequisites, degenerate systems can readily produce a distributed systemic response to local perturbations. Reciprocally, excess resources related to a single function can indirectly support multiple unrelated functions within a degenerate system. In models of genome:proteome mappings for which localized decision-making and modularity of genetic functions are assumed, we verify that such distributed compensatory effects cause enhanced robustness of system traits. The conditions needed for networked buffering to occur are neither demanding nor rare, supporting the conjecture that degeneracy may fundamentally underpin distributed robustness within several biotic and abiotic systems. For instance, networked buffering offers new insights into systems engineering and planning activities that occur under high uncertainty. It may also help explain recent developments in understanding the origins of resilience within complex ecosystems. \ud \u

Impact of the Food Additive Titanium Dioxide (E171) on Gut Microbiota-Host Interaction

The interaction between gut microbiota and host plays a central role in health. Dysbiosis, detrimental changes in gut microbiota and inflammation have been reported in non-communicable diseases. While diet has a profound impact on gut microbiota composition and function, the role of food additives such as titanium dioxide (TiO2), prevalent in processed food, is less established. In this project, we investigated the impact of food grade TiO2 on gut microbiota of mice when orally administered via drinking water. While TiO2 had minimal impact on the composition of the microbiota in the small intestine and colon, we found that TiO2 treatment could alter the release of bacterial metabolites in vivo and affect the spatial distribution of commensal bacteria in vitro by promoting biofilm formation. We also found reduced expression of the colonic mucin 2 gene, a key component of the intestinal mucus layer, and increased expression of the beta defensin gene, indicating that TiO2 significantly impacts gut homeostasis. These changes were associated with colonic inflammation, as shown by decreased crypt length, infiltration of CD8+ T cells, increased macrophages as well as increased expression of inflammatory cytokines. These findings collectively show that TiO2 is not inert, but rather impairs gut homeostasis which may in turn prime the host for disease development

Aberrant upregulation of the glycolytic enzyme PFKFB3 in CLN7 neuronal ceroid lipofuscinosis

CLN7 neuronal ceroid lipofuscinosis is an inherited lysosomal storage neurodegenerative disease highly prevalent in children. CLN7/MFSD8 gene encodes a lysosomal membrane glycoprotein, but the biochemical processes affected by CLN7-loss of function are unexplored thus preventing development of potential treatments. Here, we found, in the Cln7∆ex2 mouse model of CLN7 disease, that failure in autophagy causes accumulation of structurally and bioenergetically impaired neuronal mitochondria. In vivo genetic approach reveals elevated mitochondrial reactive oxygen species (mROS) in Cln7∆ex2 neurons that mediates glycolytic enzyme PFKFB3 activation and contributes to CLN7 pathogenesis. Mechanistically, mROS sustains a signaling cascade leading to protein stabilization of PFKFB3, normally unstable in healthy neurons. Administration of the highly selective PFKFB3 inhibitor AZ67 in Cln7∆ex2 mouse brain in vivo and in CLN7 patients-derived cells rectifies key disease hallmarks. Thus, aberrant upregulation of the glycolytic enzyme PFKFB3 in neurons may contribute to CLN7 pathogenesis and targeting PFKFB3 could alleviate this and other lysosomal storage diseases