Gravitational dynamics in a 2+1+1 decomposed spacetime along nonorthogonal double foliations: Hamiltonian evolution and gauge fixing

Motivated by situations with temporal evolution and spatial symmetries both singled out, we develop a new 2+1+1 decomposition of spacetime, based on a nonorthogonal double foliation. Time evolution proceeds along the leaves of the spatial foliation. We identify the gravitational variables in the velocity phase-space as the 2-metric (induced on the intersection $\Sigma_{t\chi }$ of the hypersurfaces of the foliations), the 2+1 components of the spatial shift vector, together with the extrinsic curvature, normal fundamental form and normal fundamental scalar of $\Sigma _{t\chi }$, all constructed with the normal to the temporal foliation. This work generalizes a previous decomposition based on orthogonal foliations, a formalism lacking one metric variable, now reintroduced. The new metric variable is related to (i) the angle of a Lorentz-rotation between the nonorthogonal bases adapted to the foliations, and (ii) to the vorticity of these basis vectors. As a first application of the formalism, we work out the Hamiltonian dynamics of general relativity in terms of the variables identified as canonical, generalizing previous work. As a second application we present the unambiguous gauge-fixing suitable to discuss the even sector scalar-type perturbations of spherically symmetric and static spacetimes in generic scalar-tensor gravitational theories, which has been obstructed in the formalism of orthogonal double foliation.Comment: 16 pages, 4 figures, to appear in Phys. Rev.

2+1+1 GENERAL RELATIVISTIC HAMILTONIAN DYNAMICS AND GAUGE FIXING IN HORNDESKI GRAVITY

A novel 2+1+1 decomposition of space-time based on a nonorthogonal double foliation is worked out and applied for the Hamiltonian description of general relativity, recovering earlier results in the proper limit. The complexity of the formalism allows for an unambiguous gauge-fixing of spherically symmetric, static black hole perturbations in the effective field theory approach of scalar-tensor gravitational theories. This gauge choice is also the closest to the general relativistic Regge-Wheeler gauge

Minimally coupled scalar fields as imperfect fluids

We revisit the issue of the fluid description of minimally coupled scalar fields. While in a cosmological setup the interpretation of a time-evolving scalar field as a perfect fluid is well-understood, the situation is more intricate when the scalar field is static, but has a spatial gradient, a situation motivated by black hole perturbations in scalar-tensor theories. Then the scalar field is interpreted as either a particular imperfect fluid of type I or a superposition of a pair of leftgoing (incoming) and rightgoing (outgoing) null dusts with a perfect fluid. Finally, when the scalar gradient is null, it is equivalent to an imperfect fluid of type II, degenerating into null dust when the energy conditions are imposed. We also propose the suitable action in terms of the fluid pressure components for each case and discuss the variational principle for a generic class of minimally coupled scalar fields.Comment: 6 pages, to appear in Physical Review

A c-jun N-terminális kináz védő szerepe nitrogén-oxid által indukált szívizom apoptosisban = Cytoprotective role of c-jun N-terminal kinase in nitric oxide-induced cardic mycocyte apoptosis

A pályázat 4 éves futamideje alatt kettős célt próbáltunk teljesíteni. 1, Az alapkutatás módszereivel sejttenyészeteken vizsgáltunk a szívizomsejtek programozott sejthalálát, az intracelluláris jelátviteli mechanizmusokra koncentrálva. Az általunk kidolgozott in vitro szepszis modellen az vizsgáltuk, hogy a nitrogén-oxidhoz (NO) hasonlóan a Gram-negatív baktériumok sejtfalából származó endotoxin (LPS) is fokozza-e a szívizomsejtek apoptotikus sejtpusztulásának arányát. Kimutattuk, hogy az LPS indukálja a szívizomsejtek programozott sejthalálát az NO termelődés fokozásán keresztül. A c-Jun N-terminális kináz (JNK) szerepét vizsgálva azt találtuk, hogy a JNK-nak kifejezett védő szerepe van a folyamatban. Az intracelluláris jelátviteli utakat vizsgálva kimutattuk, hogy az LPS az un. intrinsic apoptosis utat aktiválja. 2, A projekt második részében a szívizomsejtek regenerációs képességét vizsgáltuk szívizom infarktus után. Kidolgoztuk a humán szívizom apoptosis és perkután koronária intervenció disznó modelljét, és vizsgáltuk az infarktusos terület kiterjedésének csökkenthetőségét. Megállapítottuk, hogy mind az intrakoronáriás autológ csontvelői őssejt transzplantáció, mind a távirányított ischaemiás posztkondicionálás szignifikáns mértékben csökkenti az infarktusos terület nagyságát. | During the period of four years, two goals were tried to achieve: 1, With basic science methods, the apoptotic death of cardiac myocytes were studied on cell cultures concentrating on the intracellular signalling pathways. On an in vitro sepsis model, it was analysed whether endotoxine (LPS), like nitric oxide (NO), induces apoptotic cell death. It was shown that LPS induces apoptotic cell death through NO production. Analysing the role of c-Jun N-terminal kinase (JNK) it was revealed the JNK has a protective role in the process. Studiing the intracellular signalling pathways it was shown that LPS activates the intrinsic apoptotic pathway. 2, In the second part of the project, the regeneration capabilities of cardiac myocytes were studied after myocardial infarction. The swine model of human myocardial infarction and pimary percutaneous coronary intervention was worked out and the reduction of infarct territory was analysed. It was revealed that both the intracoronary autologous bone marrow-derived stem cell transplantation and the remote ischemic postconditioning significantly decreases the infarct territory

Central P2Y12 receptor blockade alleviates inflammatory and neuropathic pain and cytokine production in rodents.

In this study the role of P2Y12 receptors (P2Y12R) was explored in rodent models of inflammatory and neuropathic pain and in acute thermal nociception. In correlation with their activity to block the recombinant human P2Y12R, the majority of P2Y12R antagonists alleviated mechanical hyperalgesia dose-dependently, following intraplantar CFA injection, and after partial ligation of the sciatic nerve in rats. They also caused an increase in thermal nociceptive threshold in the hot plate test. Among the six P2Y12R antagonists evaluated in the pain studies, the selective P2Y12 receptor antagonist PSB-0739 was most potent upon intrathecal application. P2Y12R mRNA and IL-1beta protein were time-dependently overexpressed in the rat hind paw and lumbar spinal cord following intraplantar CFA injection. This was accompanied by the upregulation of TNF-alpha, IL-6 and IL-10 in the hind paw. PSB-0739 (0.3mg/kg i.t.) attenuated CFA-induced expression of cytokines in the hind paw and of IL-1beta in the spinal cord. Subdiaphragmatic vagotomy and the alpha7 nicotinic acetylcholine receptor antagonist MLA occluded the effect of PSB-0739 (i.t.) on pain behavior and peripheral cytokine induction. Denervation of sympathetic nerves by 6-OHDA pretreatment did not affect the action of PSB-0739. PSB-0739, in an analgesic dose, did not influence motor coordination and platelet aggregation. Genetic deletion of the P2Y12R in mice reproduced the effect of P2Y12R antagonists on mechanical hyperalgesia in inflammatory and neuropathic pain models, on acute thermal nociception and on the induction of spinal IL-1beta. Here we report the robust involvement of the P2Y12R in inflammatory pain. The anti-hyperalgesic effect of P2Y12R antagonism could be mediated by the inhibition of both central and peripheral cytokine production and involves alpha7-receptor mediated efferent pathways

Enhancing ultrafiltration performance for dairy wastewater treatment using a 3D printed turbulence promoter

Dairy factories annually generate an increasing amount of wastewater, which can cause eutrophication due to high concentrations of amino acids and lipids. To address this issue, membrane technology has emerged as a promising solution, but membrane fouling remains a significant challenge, since it can cause decreased flux, decrease membrane rejection performance, and increased energy demand. This study aimed to reduce membrane fouling by integrated a three-dimensional printed (3DP) turbulence promoter into an ultrafiltration dead-end cell and varying stirring speeds. Two mathematical models, Hermia and resistance-in-series, were used to analyze the fouling process. According to both models, the cake layer formation model indicated the most prevalent fouling mechanism. Specific energy demand, permeate flux, membrane rejection, and membrane reversible and irreversible resistances were measured, calculated, and compared. The results suggest that the combination of an integrated 3DP turbulence promoter and high stirring speeds can effectively reduce membrane fouling in a dairy wastewater treatment module

Reaction of β-Bromo-β,γ-unsaturated Pyrroline Nitroxide Aldehydes and Nitriles with Aromatic N-Binucleophiles and S-Binucleophiles

Reactions of β-bromo-β,γ-unsaturated pyrroline nitroxide aldehyde (1) or nitrile (4) or their diamagnetic forms (5, 6) with 2-aminothiophenol or 2-mercaptobenzimidazole were evaluated. The reaction could be reproduced more easily with the application of O-acetyl derivatives of nitroxides to generate 2- substituted-benzothiazole, pyrrolo[3,4-b]benzo[1,5]tiazepine scaffolds with 2-aminothiophenol and benzimidazo[2,1-b]pyrrolo[3,4-e]-[1,3]thiazine scaffold with 2-mercaptobenzimidazole

Corneal Densitometry and In Vivo Confocal Microscopy in Patients with Monoclonal Gammopathy—Analysis of 130 Eyes of 65 Subjects

Background: Corneal imaging may support an early diagnosis of monoclonal gammopathy. The goal of our study was to analyze corneal stromal properties using Pentacam and in vivo confocal cornea microscopy (IVCM) in subjects with monoclonal gammopathy. Patients and methods: In our cross-sectional study, patients with monoclonal gammopathy (130 eyes of 65 patients (40.0% males; age 67.65 ± 9.74 years)) and randomly selected individuals of the same age group, without hematological disease (100 eyes of 50 control subjects (40.0% males; age 60.67 ± 15.06 years)) were included. Using Pentacam (Pentacam HR; Oculus GmbH, Wetzlar, Germany), corneal stromal light scattering values were obtained (1) centrally 0–2 mm zone; (2) 2–6 mm zone; (3) 6–10 mm zone; (4) 10–12 mm zone. Using IVCM with Heidelberg Retina Tomograph with Rostock Cornea Module (Heidelberg Engineering, Heidelberg, Germany), the density of hyperreflective keratocytes and the number of hyperreflective spikes per image were manually analyzed, in the stroma. Results: In the first, second and third annular zone, light scattering was significantly higher in subjects with monoclonal gammopathy, than in controls (p ≤ 0.04). The number of hyperreflective keratocytes and hyperreflective spikes per image was significantly higher in stroma of subjects with monoclonal gammopathy (p ≤ 0.012). Conclusions: Our study confirms that increased corneal light scattering in the central 10 mm annular zone and increased keratocyte hyperreflectivity may give rise to suspicion of monoclonal gammopathy. As corneal light scattering is not increased at the limbal 10–12 mm annular zone in monoclonal gammopathy subjects, our spatial analysis provides evidence against the limbal origin of corneal paraprotein deposition. Using IVCM, stromal hyperreflective spikes may represent specific signs of monoclonal gammopathy