Dirac quantization of membrane in time dependent orbifold

We present quantum theory of a membrane propagating in the vicinity of a time dependent orbifold singularity. The dynamics of a membrane, with the parameters space topology of a torus, winding uniformly around compact dimension of the embedding spacetime is mathematically equivalent to the dynamics of a closed string in a flat FRW spacetime. The construction of the physical Hilbert space of a membrane makes use of the kernel space of self-adjoint constraint operators. It is a subspace of the representation space of the constraints algebra. There exist non-trivial quantum states of a membrane evolving across the singularity.Comment: 16 pages, no figures, version accepted for publication in Journal of High Energy Physic

Runx1 Expression Marks Long-Term Repopulating Hematopoietic Stem Cells in the Midgestation Mouse Embryo

AbstractHematopoietic stem cells (HSCs) are first found in the aorta-gonad-mesonephros region and vitelline and umbilical arteries of the midgestation mouse embryo. Runx1 (AML1), the DNA binding subunit of a core binding factor, is required for the emergence and/or subsequent function of HSCs. We show that all HSCs in the embryo express Runx1. Furthermore, HSCs in Runx1+/− embryos are heterogeneous and include CD45+ cells, endothelial cells, and mesenchymal cells. Comparison with wild-type embryos showed that the distribution of HSCs among these various cell populations is sensitive to Runx1 dosage. These data provide the first morphological description of embryonic HSCs and contribute new insight into their cellular origin

Observational hints on the Big Bounce

In this paper we study possible observational consequences of the bouncing cosmology. We consider a model where a phase of inflation is preceded by a cosmic bounce. While we consider in this paper only that the bounce is due to loop quantum gravity, most of the results presented here can be applied for different bouncing cosmologies. We concentrate on the scenario where the scalar field, as the result of contraction of the universe, is driven from the bottom of the potential well. The field is amplified, and finally the phase of the standard slow-roll inflation is realized. Such an evolution modifies the standard inflationary spectrum of perturbations by the additional oscillations and damping on the large scales. We extract the parameters of the model from the observations of the cosmic microwave background radiation. In particular, the value of inflaton mass is equal to $m=(2.6 \pm 0.6) \cdot 10^{13}$ GeV. In our considerations we base on the seven years of observations made by the WMAP satellite. We propose the new observational consistency check for the phase of slow-roll inflation. We investigate the conditions which have to be fulfilled to make the observations of the Big Bounce effects possible. We translate them to the requirements on the parameters of the model and then put the observational constraints on the model. Based on assumption usually made in loop quantum cosmology, the Barbero-Immirzi parameter was shown to be constrained by $\gamma<1100$ from the cosmological observations. We have compared the Big Bounce model with the standard Big Bang scenario and showed that the present observational data is not informative enough to distinguish these models.Comment: 25 pages, 8 figures, JHEP3.cl

Evolution in bouncing quantum cosmology

We present the method of describing an evolution in quantum cosmology in the framework of the reduced phase space quantization of loop cosmology. We apply our method to the flat Friedman-Robertson-Walker model coupled to a massless scalar field. We identify the physical quantum Hamiltonian that is positive-definite and generates globally an unitary evolution of considered quantum system. We examine properties of expectation values of physical observables in the process of the quantum big bounce transition. The dispersion of evolved observables are studied for the Gaussian state. Calculated relative fluctuations enable an examination of the semi-classicality conditions and possible occurrence of the cosmic forgetfulness. Preliminary estimations based on the cosmological data suggest that there was no cosmic amnesia. Presented results are analytical, and numerical computations are only used for the visualization purposes. Our method may be generalized to sophisticated cosmological models including the Bianchi type universes.Comment: 28 pages, 7 figures. Matches version published in Class. Quantum Gra

Omental and pleural milky spots: different reactivity patterns in mice infected with Schistosoma mansoni reveals coelomic compartmentalisation

In vertebrate animals, pleural and peritoneal cavities are repositories of milky spots (MS), which constitute an organised coelom-associated lymphomyeloid tissue that is intensively activated by Schistosoma mansoni infection. This study compared the reactive patterns of peritoneal MS to pleural MS and concluded from histological analysis that they represent independent responsive compartments. Whole omentum, lungs and the entire mediastinum of 54 S. mansoni-infected mice were studied morphologically. The omental MS of infected animals were highly activated, modulating from myeloid-lymphocytic (60 days of infection) to lymphomyeloid (90 days of infection) and lymphocytic or lymphoplasmacytic (160 days of infection) types. The non-lymphoid component predominated in the acute phase of infection and was expressed by monocytopoietic, eosinopoietic and neutropoietic foci, with isolated megakaryocytes and small foci of late normoblasts and mast cells. Nevertheless, pleural or thoracic MS of infected mice were monotonous, consisting of small and medium lymphocytes with few mast and plasma cells and no myeloid component. Our data indicate that compartmentalisation of the MS response is dependent on the lymphatic vascularisation of each coelomic cavity, limiting the effects or consequences of any stimulating or aggressive agents, as is the case with S. mansoni infection

Sequential morphological characteristics of murine fetal liver hematopoietic microenvironment in Swiss Webster mice

Embryonic hematopoiesis occurs via dynamic development with cells migrating into various organs. Fetal liver is the main hematopoietic organ responsible for hematopoietic cell expansion during embryologic development. We describe the morphological sequential characteristics of murine fetal liver niches that favor the settlement and migration of hematopoietic cells from 12 days post-coitum (dpc) to 0 day post-partum. Liver sections were stained with hematoxylin and eosin, Lennert’s Giemsa, Sirius Red pH 10.2, Gomori’s Reticulin, and Periodic Acid Schiff/Alcian Blue pH 1.0 and pH 2.5 and were analyzed by bright-field microscopy. Indirect imunohistochemistry for fibronectin, matrix metalloproteinase-1 (MMP-1), and MMP-9 and histochemistry for naphthol AS-D chloroacetate esterase (NCAE) were analyzed by confocal microscopy. The results showed that fibronectin was related to the promotion of hepatocyte and trabecular differentiation; reticular fibers did not appear to participate in fetal hematopoiesis but contributed to the physical support of the liver after 18 dpc. During the immature phase, hepatocytes acted as the fundamental stroma for the erythroid lineage. The appearance of myeloid cells in the liver was related to perivascular and subcapsular collagen, and NCAE preceded MMP-1 expression in neutrophils, an occurrence that appeared to contribute to their liver evasion. Thus, the murine fetal liver during ontogenesis shows two different phases: one immature and mainly endodermic (<14 dpc) and the other more developed (endodermic-mesenchymal; >15 dpc) with the maturation of hepatocytes, a better definition of trabecular pattern, and an increase in the connective tissue in the capsule, portal spaces, and liver parenchyma. The decrease of hepatic hematopoiesis (migration) coincides with hepatic maturation

Hematopoietic Stem Cell Development Is Dependent on Blood Flow

SummaryDuring vertebrate embryogenesis, hematopoietic stem cells (HSCs) arise in the aorta-gonads-mesonephros (AGM) region. We report here that blood flow is a conserved regulator of HSC formation. In zebrafish, chemical blood flow modulators regulated HSC development, and silent heart (sih) embryos, lacking a heartbeat and blood circulation, exhibited severely reduced HSCs. Flow-modifying compounds primarily affected HSC induction after the onset of heartbeat; however, nitric oxide (NO) donors regulated HSC number even when treatment occurred before the initiation of circulation, and rescued HSCs in sih mutants. Morpholino knockdown of nos1 (nnos/enos) blocked HSC development, and its requirement was shown to be cell autonomous. In the mouse, Nos3 (eNos) was expressed in HSCs in the AGM. Intrauterine Nos inhibition or embryonic Nos3 deficiency resulted in a reduction of hematopoietic clusters and transplantable murine HSCs. This work links blood flow to AGM hematopoiesis and identifies NO as a conserved downstream regulator of HSC development

Expression analysis of the TAB2 protein in adult mouse tissues

Background: The Interleukin-1 (IL-1) signaling component TAK1 binding protein 2 (TAB2) plays a role in activating the NFκB and JNK signaling pathways. Additionally, TAB2 functions in the nucleus as a repressor of NFκB-mediated gene regulation. Objective: To obtain insight into the function of TAB2 in the adult mouse, we analyzed the in vivo TAB2 expression pattern. Materials and methods: Cell lines and adult mouse tissues were analyzed for TAB2 protein expression and localization. Results: Immunohistochemical staining for TAB2 protein revealed expression in the vascular endothelium of most tissues, hematopoietic cells and brain cells. While TAB2 is localized in both the nucleus and the cytoplasm in cell lines, cytoplasmic localization predominates in hematopoietic tissues in vivo. Conclusions: The TAB2 expression pattern shows striking similarities with previously reported IL-1 receptor expression and NFκB activation patterns, suggesting that TAB2 in vivo is playing a role in these signaling pathways

Wnt3a deficiency irreversibly impairs hematopoietic stem cell self-renewal and leads to defects in progenitor cell differentiation

Canonical Wnt signaling has been implicated in various aspects of hematopoiesis. Its role is controversial due to different outcomes between various inducible Wnt-signaling loss-of-function models and also compared with gain-of-function systems. We therefore studied a mouse deficient for a Wnt gene that seemed to play a nonredundant role in hematopoiesis. Mice lacking Wnt3a die prenatally around embryonic day (E) 12.5, allowing fetal hematopoiesis to be studied using in vitro assays and transplantation into irradiated recipient mice. Here we show that Wnt3a deficiency leads to a reduction in the numbers of hematopoietic stem cells (HSCs) and progenitor cells in the fetal liver (FL) and to severely reduced reconstitution capacity as measured in secondary transplantation assays. This deficiency is irreversible and cannot be restored by transplantation into Wnt3a competent mice. The impaired long-term repopulation capacity of Wnt3a-/- HSCs could not be explained by altered cell cycle or survival of primitive progenitors. Moreover, Wnt3a deficiency affected myeloid but not B-lymphoid development at the progenitor level, and affected immature thymocyte differentiation. Our results show that Wnt3a signaling not only provides proliferative stimuli, such as for immature thymocytes, but also regulates cell fate decisions of HSC during hematopoiesis

An actionable guide to creating Educational Escape Rooms: handbook

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