The back reaction and the effective Einstein's equation for the Universe with ideal fluid cosmological perturbations

We investigate the back reaction of cosmological perturbations on the evolution of the Universe using the renormalization group method. Starting from the second order perturbed Einstein's equation, we renormalize a scale factor of the Universe and derive the evolution equation for the effective scale factor which includes back reaction due to inhomogeneities of the Universe. The resulting equation has the same form as the standard Friedman-Robertson-Walker equation with the effective energy density and pressure which represent the back reaction effect.Comment: 16 pages, to appear in Phys. Rev.

Back Reaction Problem in the Inflationary Universe

We investigate the back reaction of cosmological perturbations on an inflationary universe using the renormalization-group method. The second-order zero mode solution which appears by the nonlinearity of the Einstein equation is regarded as a secular term of a perturbative expansion, we renormalized a constant of integration contained in the background solution and absorbed the secular term to this constant in a gauge-invariant manner. The resultant renormalization-group equation describes the back reaction effect of inhomogeneity on the background universe. For scalar type classical perturbation, by solving the renormalization-group equation, we find that the back reaction of the long wavelength fluctuation works as a positive spatial curvature, and the short wavelength fluctuation works as a radiation fluid. For the long wavelength quantum fluctuation, the effect of back reaction is equivalent to a negative spatial curvature.Comment: 17 page

Renormalization Group Approach to Cosmological Back Reaction Problems

We investigated the back reaction of cosmological perturbations on the evolution of the universe using the second order perturbation of the Einstein's equation. To incorporate the back reaction effect due to the inhomogeneity into the framework of the cosmological perturbation, we used the renormalization group method. The second order zero mode solution which appears by the non-linearities of the Einstein's equation is regarded as a secular term of the perturbative expansion, we renormalized a constant of integration contained in the background solution and absorbed the secular term to this constant. For a dust dominated universe, using the second order gauge invariant quantity, we derived the renormalization group equation which determines the effective dynamics of the Friedman-Robertson-Walker universe with the back reaction effect in a gauge invariant manner. We obtained the solution of the renormalization group equation and found that perturbations of the scalar mode and the long wavelength tensor mode works as positive spatial curvature, and the short wavelength tensor mode as radiation fluid.Comment: 18 pages, revtex, to appear in Phys. Rev.

Immunological aspects in chronic lymphocytic leukemia (CLL) development

Chronic lymphocytic leukemia (CLL) is unique among B cell malignancies in that the malignant clones can be featured either somatically mutated or unmutated IGVH genes. CLL cells that express unmutated immunoglobulin variable domains likely underwent final development prior to their entry into the germinal center, whereas those that express mutated variable domains likely transited through the germinal center and then underwent final development. Regardless, the cellular origin of CLL remains unknown. The aim of this review is to summarize immunological aspects involved in this process and to provide insights about the complex biology and pathogenesis of this disease. We propose a mechanistic hypothesis to explain the origin of B-CLL clones into our current picture of normal B cell development. In particular, we suggest that unmutated CLL arises from normal B cells with self-reactivity for apoptotic bodies that have undergone receptor editing, CD5 expression, and anergic processes in the bone marrow. Similarly, mutated CLL would arise from cells that, while acquiring self-reactivity for autoantigens—including apoptotic bodies—in germinal centers, are also still subject to tolerization mechanisms, including receptor editing and anergy. We believe that CLL is a proliferation of B lymphocytes selected during clonal expansion through multiple encounters with (auto)antigens, despite the fact that they differ in their state of activation and maturation. Autoantigens and microbial pathogens activate BCR signaling and promote tolerogenic mechanisms such as receptor editing/revision, anergy, CD5+ expression, and somatic hypermutation in CLL B cells. The result of these tolerogenic mechanisms is the survival of CLL B cell clones with similar surface markers and homogeneous gene expression signatures. We suggest that both immunophenotypic surface markers and homogenous gene expression might represent the evidence of several attempts to re-educate self-reactive B cells

NK-cell receptors NKp46 and NCR1 control human metapneumovirus infection.

Natural killer (NK) cells are capable of killing various pathogens upon stimulation of activating receptors. Human metapneumovirus (HMPV) is a respiratory virus, which was discovered in 2001 and is responsible for acute respiratory tract infection in infants and children worldwide. HMPV infection is very common, infecting around 70% of all children under the age of five. Under immune suppressive conditions, HMPV infection can be fatal. Not much is known on how NK cells respond to HMPV. In this study, using reporter assays and NK-cell cytotoxicity assays performed with human and mouse NK cells, we demonstrated that the NKp46-activating receptor and its mouse orthologue Ncr1, both members of the natural cytotoxicity receptor (NCR) family, recognized an unknown ligand expressed by HMPV-infected human cells. We demonstrated that MHC class I is upregulated and MICA is downregulated upon HMPV infection. We also characterized mouse NK-cell phenotype in the blood and the lungs of HMPV-infected mice and found that lung NK cells are more activated and expressing NKG2D, CD43, CD27, KLRG1, and CD69 compared to blood NK cells regardless of HMPV infection. Finally, we demonstrated, using Ncr1-deficient mice, that NCR1 plays a critical role in controlling HMPV infection