From Poincare to affine invariance: How does the Dirac equation generalize?

A generalization of the Dirac equation to the case of affine symmetry, with SL(4,R) replacing SO(1,3), is considered. A detailed analysis of a Dirac-type Poincare-covariant equation for any spin j is carried out, and the related general interlocking scheme fulfilling all physical requirements is established. Embedding of the corresponding Lorentz fields into infinite-component SL(4,R) fermionic fields, the constraints on the SL(4,R) vector-operator generalizing Dirac's gamma matrices, as well as the minimal coupling to (Metric-)Affine gravity are studied. Finally, a symmetry breaking scenario for SA(4,R) is presented which preserves the Poincare symmetry.Comment: 34 pages, LaTeX2e, 8 figures, revised introduction, typos correcte

SLˉ(4,R)\bar{SL}(4,R) Embedding for a 3D World Spinor Equation

A generic-curved spacetime Dirac-like equation in 3D is constructed. It has, owing to the $\bar{SL}(n,R)$ group deunitarizing automorphism, a physically correct unitarity and flat spacetime particle properties. The construction is achieved by embedding $\bar{SL}(3,R)$ vector operator $X_{\mu}$, that plays a role of Dirac's $\gamma_{\mu}$ matrices, into $\bar{SL}(4,R)$. Decomposition of the unitary irreducible spinorial $\bar{SL}(4,R)$ representations gives rise to an explicit form of the infinite $X_{\mu}$ matrices

A Higgs Mechanism for Gravity

In this paper we elaborate on the idea of an emergent spacetime which arises due to the dynamical breaking of diffeomorphism invariance in the early universe. In preparation for an explicit symmetry breaking scenario, we consider nonlinear realizations of the group of analytical diffeomorphisms which provide a unified description of spacetime structures. We find that gravitational fields, such as the affine connection, metric and coordinates, can all be interpreted as Goldstone fields of the diffeomorphism group. We then construct a Higgs mechanism for gravity in which an affine spacetime evolves into a Riemannian one by the condensation of a metric. The symmetry breaking potential is identical to that of hybrid inflation but with the non-inflaton scalar extended to a symmetric second rank tensor. This tensor is required for the realization of the metric as a Higgs field. We finally comment on the role of Goldstone coordinates as a dynamical fluid of reference.Comment: 15 pages, 2 figures, 3 tables, appendix C on on-shell d.o.f. added, references adde

Holographic Approach to Regge Trajectory and Rotating D5 brane

We study the Regge trajectories of holographic mesons and baryons by considering rotating strings and D5 brane, which is introduced as the baryon vertex. Our model is based on the type IIB superstring theory with the background of asymptotic $AdS_5\times S^5$. This background is dual to a confining supersymmetric Yang-Mills theory (SYM) with gauge condensate, $$, which determines the tension of the linear potential between the quark and anti-quark. Then the slope of the meson trajectory ($\alpha'_{M}$) is given by this condensate as $\alpha'_{M}=1/\sqrt{\pi }$ at large spin $J$. This relation is compatible with the other theoretical results and experiments. For the baryon, we show the importance of spinning baryon vertex to obtain a Regge slope compatible with the one of $N$ and $\Delta$ series. In both cases, mesons and baryons, the trajectories are shifted to large mass side with the same slope for increasing current quark mass.Comment: 28 pages, 7 figure

DNM1 encephalopathy: A new disease of vesicle fission.

ObjectiveTo evaluate the phenotypic spectrum caused by mutations in dynamin 1 (DNM1), encoding the presynaptic protein DNM1, and to investigate possible genotype-phenotype correlations and predicted functional consequences based on structural modeling.MethodsWe reviewed phenotypic data of 21 patients (7 previously published) with DNM1 mutations. We compared mutation data to known functional data and undertook biomolecular modeling to assess the effect of the mutations on protein function.ResultsWe identified 19 patients with de novo mutations in DNM1 and a sibling pair who had an inherited mutation from a mosaic parent. Seven patients (33.3%) carried the recurrent p.Arg237Trp mutation. A common phenotype emerged that included severe to profound intellectual disability and muscular hypotonia in all patients and an epilepsy characterized by infantile spasms in 16 of 21 patients, frequently evolving into Lennox-Gastaut syndrome. Two patients had profound global developmental delay without seizures. In addition, we describe a single patient with normal development before the onset of a catastrophic epilepsy, consistent with febrile infection-related epilepsy syndrome at 4 years. All mutations cluster within the GTPase or middle domains, and structural modeling and existing functional data suggest a dominant-negative effect on DMN1 function.ConclusionsThe phenotypic spectrum of DNM1-related encephalopathy is relatively homogeneous, in contrast to many other genetic epilepsies. Up to one-third of patients carry the recurrent p.Arg237Trp variant, which is now one of the most common recurrent variants in epileptic encephalopathies identified to date. Given the predicted dominant-negative mechanism of this mutation, this variant presents a prime target for therapeutic intervention

Exploring Norms in Agile Software Teams

The majority of software developers work in teams and are thus influenced by team norms. Norms are shared expectations of how to behave and regulate the interaction between team members. Our aim of this study is to gain more knowledge about team norms in software teams and to increase the understanding of how norms influence teamwork in agile software development projects. We conducted a study of norms in four agile teams located in Norway and Malaysia. The analysis of 22 interviews revealed that we could extract a varied set of both injunctive and descriptive norms. Our results suggest that team norms have an important role in enabling team performance.acceptedVersio

Novel study designs to investigate the placebo response

<p>Abstract</p> <p>Background</p> <p>Investigating the size and mechanisms of the placebo response in clinical trials have relied on experimental procedures that simulate the double-blind randomized placebo-controlled design. However, as the conventional design is thought to elucidate drug rather than placebo actions, different methodological procedures are needed for the placebo response.</p> <p>Methods</p> <p>We reviewed the respective literature for trials designs that may be used to elucidate the size of the placebo response and the mechanisms associated with it.</p> <p>Results</p> <p>In general, this can be done by either manipulation the information provided to the subjects, or by manipulation the timing of the drug applied. Two examples of each strategy are discussed: the "balanced placebo design" (BDP) and the "balanced cross-over design" (BCD) and their variants are based on false information, while the "hidden treatment" (HT) and the ""delayed response test" (DRT) are based on manipulating the time of drug action. Since most such approaches include deception or incomplete information of the subjects they are suitable for patient only with authorized deception.</p> <p>Conclusion</p> <p>Both manipulating the information provided to subjects (BDP, DCD) or manipulating the timing of drug application (HT, DRT) allows overcoming some of the restrictions of conventional drug trials in the assessment of the placebo response, but they are feasible mostly in healthy subjects for ethical reasons.</p

In Vitro and Sensory Evaluation of Capsaicin-Loaded Nanoformulations

Capsaicin has known health beneficial and therapeutic properties. It is also able to enhance the permeability of drugs across epithelial tissues. Unfortunately, due to its pungency the oral administration of capsaicin is limited. To this end, we assessed the effect of nanoencapsulation of capsaicin, under the hypothesis that this would reduce its pungency. Core-shell nanocapsules with an oily core and stabilized with phospholipids were used. This system was used with or without chitosan coating. In this work, we investigated the in vitro release behavior of capsaicin-loaded formulations in different physiological media (including simulated saliva fluid). We also evaluated the influence of encapsulation of capsaicin on the cell viability of buccal cells (TR146). To study the changes in pungency after encapsulation we carried out a sensory analysis with a trained panel of 24 students. The in vitro release study showed that the systems discharged capsaicin slowly in a monotonic manner and that the chitosan coating had an effect on the release profile. The cytotoxic response of TR146 cells to capsaicin at a concentration of 500 μM, which was evident for the free compound, was reduced following its encapsulation. The sensory study revealed that a chitosan coating results in a lower threshold of perception of the formulation. The nanoencapsulation of capsaicin resulted in attenuation of the sensation of pungency significantly. However, the presence of a chitosan shell around the nanoformulations did not mask the pungency, when compared with uncoated systems

Can Research Assessments Themselves Cause Bias in Behaviour Change Trials? A Systematic Review of Evidence from Solomon 4-Group Studies

BACKGROUND: The possible effects of research assessments on participant behaviour have attracted research interest, especially in studies with behavioural interventions and/or outcomes. Assessments may introduce bias in randomised controlled trials by altering receptivity to intervention in experimental groups and differentially impacting on the behaviour of control groups. In a Solomon 4-group design, participants are randomly allocated to one of four arms: (1) assessed experimental group; (2) unassessed experimental group (3) assessed control group; or (4) unassessed control group. This design provides a test of the internal validity of effect sizes obtained in conventional two-group trials by controlling for the effects of baseline assessment, and assessing interactions between the intervention and baseline assessment. The aim of this systematic review is to evaluate evidence from Solomon 4-group studies with behavioural outcomes that baseline research assessments themselves can introduce bias into trials. METHODOLOGY/PRINCIPAL FINDINGS: Electronic databases were searched, supplemented by citation searching. Studies were eligible if they reported appropriately analysed results in peer-reviewed journals and used Solomon 4-group designs in non-laboratory settings with behavioural outcome measures and sample sizes of 20 per group or greater. Ten studies from a range of applied areas were included. There was inconsistent evidence of main effects of assessment, sparse evidence of interactions with behavioural interventions, and a lack of convincing data in relation to the research question for this review. CONCLUSIONS/SIGNIFICANCE: There were too few high quality completed studies to infer conclusively that biases stemming from baseline research assessments do or do not exist. There is, therefore a need for new rigorous Solomon 4-group studies that are purposively designed to evaluate the potential for research assessments to cause bias in behaviour change trials

Bcl-2 protein family: Implications in vascular apoptosis and atherosclerosis

Apoptosis has been recognized as a central component in the pathogenesis of atherosclerosis, in addition to the other human pathologies such as cancer and diabetes. The pathophysiology of atherosclerosis is complex, involving both apoptosis and proliferation at different phases of its progression. Oxidative modification of lipids and inflammation differentially regulate the apoptotic and proliferative responses of vascular cells during progression of the atherosclerotic lesion. Bcl-2 proteins act as the major regulators of extrinsic and intrinsic apoptosis signalling pathways and more recently it has become evident that they mediate the apoptotic response of vascular cells in response to oxidation and inflammation either in a provocative or an inhibitory mode of action. Here we address Bcl-2 proteins as major therapeutic targets for the treatment of atherosclerosis and underscore the need for the novel preventive and therapeutic interventions against atherosclerosis, which should be designed in the light of molecular mechanisms regulating apoptosis of vascular cells in atherosclerotic lesions