216 research outputs found
Perturbative instabilities in Horava gravity
We investigate the scalar and tensor perturbations in Horava gravity, with
and without detailed balance, around a flat background. Once both types of
perturbations are taken into account, it is revealed that the theory is plagued
by ghost-like scalar instabilities in the range of parameters which would
render it power-counting renormalizable, that cannot be overcome by simple
tricks such as analytic continuation. Implementing a consistent flow between
the UV and IR limits seems thus more challenging than initially presumed,
regardless of whether the theory approaches General Relativity at low energies
or not. Even in the phenomenologically viable parameter space, the tensor
sector leads to additional potential problems, such as fine-tunings and
super-luminal propagation.Comment: 21 pages, version published at Class. Quant. Gra
The Changes in China's Forests: An Analysis Using the Forest Identity
Changes in forest carbon stocks are a determinant of the regional carbon budget. In the past several decades, China has experienced a pronounced increase in forest area and density. However, few comprehensive analyses have been conducted. In this study, we employed the Forest Identity concept to evaluate the changing status of China's forests over the past three decades, using national forest inventory data of five periods (1977â1981, 1984â1988, 1989â1993, 1994â1998, and 1999â2003). The results showed that forest area and growing stock density increased by 0.51% and 0.44% annually over the past three decades, while the conversion ratio of forest biomass to growing stock declined by 0.10% annually. These developments resulted in a net annual increase of 0.85% in forest carbon sequestration, which is equivalent to a net biomass carbon uptake of 43.8 Tg per year (1 Tgâ=â1012 g). This increase can be attributed to the national reforestation/afforestation programs, environmentally enhanced forest growth and economic development as indicated by the average gross domestic product
Horava-Lifshitz Holography
We derive the detailed balance condition as a solution to the Hamilton-Jacobi
equation in the Horava-Lifshitz gravity. This result leads us to propose the
existence of the d-dimensional quantum field theory on the future boundary of
the (d+1)-dimensional Horava-Lifshitz gravity from the viewpoint of the
holographic renormalization group. We also obtain a Ricci flow equation of the
boundary theory as the holographic RG flow, which is the Hamilton equation in
the bulk gravity, by tuning parameters in the theory.Comment: 7 page
Pulmonary Arterial Hypertension Affects the Rat Gut Microbiome
We have analysed whether pulmonary arterial hypertension (PAH) alters the rat faecal microbiota.
Wistar rats were injected with the VEGF receptor antagonist SU5416 (20 mg/kg s.c.) and followed
for 2 weeks kept in hypoxia (10% O2, PAH) or injected with vehicle and kept in normoxia (controls).
Faecal samples were obtained and microbiome composition was determined by 16S rRNA gene
sequencing and bioinformatic analysis. No effect of PAH on the global microbiome was found (α- or
ÎČ-diversity). However, PAH-exposed rats showed gut dysbiosis as indicated by a taxonomy-based
analysis. Specifically, PAH rats had a three-fold increase in Firmicutes-to-Bacteroidetes ratio. Within
the Firmicutes phylum, there were no large changes in the relative abundance of the bacterial families
in PAH. Among Bacteroidetes, all families were less abundant in PAH. A clear separation was observed
between the control and PAH clusters based on short chain fatty acid producing bacterial genera.
Moreover, acetate was reduced in the serum of PAH rats. In conclusion, faecal microbiota composition is
altered as a result of PAH. This misbalanced bacterial ecosystem might in turn play a pathophysiological
role in PAH by altering the immunologic, hormonal and metabolic homeostasis.This study is supported by grants from Mineco (SAF2014-55399-R, SAF2014-55523-R,
SAF2016-77222 and SAF2017-84494-C2-1R), Instituto de Salud Carlos III (PI15/01100), with funds from the
European Union (Fondo Europeo de Desarrollo Regional FEDER). M.C., G.M-P. and S.E-R. are funded by
Universidad Complutense, Fondo de GarantĂa Juvenil (Comunidad de Madrid) and Ciberes grant with funds
from FundaciĂłn Contra la HipertensiĂłn Pulmonar, a FPU grant from Ministerio de EducaciĂłn, respectively.
J.L.I.G is a CNIC IPP COFUND Fellow and has received funding from the People Programme (Marie Curie
Actions) of the FP7/2007-2013 under REA grant agreement n° 600396. The CNIC is supported by MEIC-AEI and
the Pro CNIC Foundation, and is a Severo Ochoa Center of Excellence (MEIC award SEV-2015-0505)
How do Regulatory T Cells Work?
CD4+ T cells are commonly divided into regulatory T (Treg) cells and conventional T helper (Th) cells. Th cells control adaptive immunity against pathogens and cancer by activating other effector immune cells. Treg cells are defined as CD4+ T cells in charge of suppressing potentially deleterious activities of Th cells. This review briefly summarizes the current knowledge in the Treg field and defines some key questions that remain to be answered. Suggested functions for Treg cells include: prevention of autoimmune diseases by maintaining self-tolerance; suppression of allergy, asthma and pathogen-induced immunopathology; feto-maternal tolerance; and oral tolerance. Identification of Treg cells remains problematic, because accumulating evidence suggests that all the presently-used Treg markers (CD25, CTLA-4, GITR, LAG-3, CD127 and Foxp3) represent general T-cell activation markers, rather than being truly Treg-specific. Treg-cell activation is antigen-specific, which implies that suppressive activities of Treg cells are antigen-dependent. It has been proposed that Treg cells would be self-reactive, but extensive TCR repertoire analysis suggests that self-reactivity may be the exception rather than the rule. The classification of Treg cells as a separate lineage remains controversial because the ability to suppress is not an exclusive Treg property. Suppressive activities attributed to Treg cells may in reality, at least in some experimental settings, be exerted by conventional Th cell subsets, such as Th1, Th2, Th17 and T follicular (Tfh) cells. Recent reports have also demonstrated that Foxp3+ Treg cells may differentiate in vivo into conventional effector Th cells, with or without concomitant downregulation of Foxp3
Nuclear Translocation of ÎČ-Catenin during Mesenchymal Stem Cells Differentiation into Hepatocytes Is Associated with a Tumoral Phenotype
Wnt/ÎČ-catenin pathway controls biochemical processes related to cell differentiation. In committed cells the alteration of this pathway has been associated with tumors as hepatocellular carcinoma or hepatoblastoma. The present study evaluated the role of Wnt/ÎČ-catenin activation during human mesenchymal stem cells differentiation into hepatocytes. The differentiation to hepatocytes was achieved by the addition of two different conditioned media. In one of them, ÎČ-catenin nuclear translocation, up-regulation of genes related to the Wnt/ÎČ-catenin pathway, such as Lrp5 and Fzd3, as well as the oncogenes c-myc and p53 were observed. While in the other protocol there was a Wnt/ÎČ-catenin inactivation. Hepatocytes with nuclear translocation of ÎČ-catenin also had abnormal cellular proliferation, and expressed membrane proteins involved in hepatocellular carcinoma, metastatic behavior and cancer stem cells. Further, these cells had also increased auto-renewal capability as shown in spheroids formation assay. Comparison of both differentiation protocols by 2D-DIGE proteomic analysis revealed differential expression of 11 proteins with altered expression in hepatocellular carcinoma. Cathepsin B and D, adenine phosphoribosyltransferase, triosephosphate isomerase, inorganic pyrophosphatase, peptidyl-prolyl cis-trans isomerase A or lactate dehydrogenase ÎČ-chain were up-regulated only with the protocol associated with Wnt signaling activation while other proteins involved in tumor suppression, such as transgelin or tropomyosin ÎČ-chain were down-regulated in this protocol. In conclusion, our results suggest that activation of the Wnt/ÎČ-catenin pathway during human mesenchymal stem cells differentiation into hepatocytes is associated with a tumoral phenotype
Regulating the transition from centriole to basal body
The role of centrioles changes as a function of the cell cycle. Centrioles promote formation of spindle poles in mitosis and act as basal bodies to assemble primary cilia in interphase. Stringent regulations govern conversion between these two states. Although the molecular mechanisms have not been fully elucidated, recent findings have begun to shed light on pathways that regulate the conversion of centrioles to basal bodies and vice versa. Emerging studies also provide insights into how defects in the balance between centrosome and cilia function could promote ciliopathies and cancer
Molecular mechanisms of cell death: recommendations of the Nomenclature Committee on Cell Death 2018.
Over the past decade, the Nomenclature Committee on Cell Death (NCCD) has formulated guidelines for the definition and interpretation of cell death from morphological, biochemical, and functional perspectives. Since the field continues to expand and novel mechanisms that orchestrate multiple cell death pathways are unveiled, we propose an updated classification of cell death subroutines focusing on mechanistic and essential (as opposed to correlative and dispensable) aspects of the process. As we provide molecularly oriented definitions of terms including intrinsic apoptosis, extrinsic apoptosis, mitochondrial permeability transition (MPT)-driven necrosis, necroptosis, ferroptosis, pyroptosis, parthanatos, entotic cell death, NETotic cell death, lysosome-dependent cell death, autophagy-dependent cell death, immunogenic cell death, cellular senescence, and mitotic catastrophe, we discuss the utility of neologisms that refer to highly specialized instances of these processes. The mission of the NCCD is to provide a widely accepted nomenclature on cell death in support of the continued development of the field
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