802 research outputs found
Avoiding catastrophic failure in correlated networks of networks
Networks in nature do not act in isolation but instead exchange information,
and depend on each other to function properly. An incipient theory of Networks
of Networks have shown that connected random networks may very easily result in
abrupt failures. This theoretical finding bares an intrinsic paradox: If
natural systems organize in interconnected networks, how can they be so stable?
Here we provide a solution to this conundrum, showing that the stability of a
system of networks relies on the relation between the internal structure of a
network and its pattern of connections to other networks. Specifically, we
demonstrate that if network inter-connections are provided by hubs of the
network and if there is a moderate degree of convergence of inter-network
connection the systems of network are stable and robust to failure. We test
this theoretical prediction in two independent experiments of functional brain
networks (in task- and resting states) which show that brain networks are
connected with a topology that maximizes stability according to the theory.Comment: 40 pages, 7 figure
Human helminth therapy to treat inflammatory disorders - where do we stand?
Parasitic helminths have evolved together with the mammalian immune system over many millennia and as such they have become remarkably efficient modulators in order to promote their own survival. Their ability to alter and/or suppress immune responses could be beneficial to the host by helping control excessive inflammatory responses and animal models and pre-clinical trials have all suggested a beneficial effect of helminth infections on inflammatory bowel conditions, MS, asthma and atopy. Thus, helminth therapy has been suggested as a possible treatment method for autoimmune and other inflammatory disorders in humans
Location of chlorogenic acid biosynthesis pathway and polyphenol oxidase genes in a new interspecific anchored linkage map of eggplant
© Gramazio et al.; licensee BioMed Central. 2014. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated
Early rheumatoid arthritis is characterized by a distinct and transient synovial fluid cytokine profile of T cell and stromal cell origin
Pathological processes involved in the initiation of rheumatoid synovitis remain unclear. We undertook the present study to identify immune and stromal processes that are present soon after the clinical onset of rheumatoid arthritis ( RA) by assessing a panel of T cell, macrophage, and stromal cell related cytokines and chemokines in the synovial fluid of patients with early synovitis. Synovial fluid was aspirated from inflamed joints of patients with inflammatory arthritis of duration 3 months or less, whose outcomes were subsequently determined by follow up. For comparison, synovial fluid was aspirated from patients with acute crystal arthritis, established RA and osteoarthritis. Rheumatoid factor activity was blocked in the synovial fluid samples, and a panel of 23 cytokines and chemokines measured using a multiplex based system. Patients with early inflammatory arthritis who subsequently developed RA had a distinct but transient synovial fluid cytokine profile. The levels of a range of T cell, macrophage and stromal cell related cytokines ( e. g. IL-2, IL-4, IL-13, IL-17, IL-15, basic fibroblast growth factor and epidermal growth factor) were significantly elevated in these patients within 3 months after symptom onset, as compared with early arthritis patients who did not develop RA. In addition, this profile was no longer present in established RA. In contrast, patients with non-rheumatoid persistent synovitis exhibited elevated levels of interferon-gamma at initiation. Early synovitis destined to develop into RA is thus characterized by a distinct and transient synovial fluid cytokine profile. The cytokines present in the early rheumatoid lesion suggest that this response is likely to influence the microenvironment required for persistent RA
Relationship between length of exposure to trauma and mental illness in the police
Introduction: The activities of the police are considered high risk, because they are exposed to high levels of physical and emotional stress. These work activities can contribute to the emergence of psychiatric disorders that affect their readiness in responding to threats and safety of their actions. Our aim was to conduct a systematic literature review to identify studies that evaluated the time that police officers may be deployed without developing a mental illness. Materials and Methods: Articles published until May 2016 in The MEDLINE (PubMed), Cochrane Library, PsycINFO, and Lilacs databases were searched. In addition, a manual search in the gray literature (theses and dissertations) was also conducted. Several combinations of indexed terms were used in the search of electronic databases, including terms referring to trauma exposure, intervention, and population. There were no restrictions on date and language of the publications. Two reviewers independently assessed studies for eligibility and quality. Disagreements were resolved after consultations with a third reviewer. Results: Of 905 selected studies, 13 studies evaluated deployment duration and the incidence of mental illness. Studies were excluded because they addressed the prevalence of mental illness but did not relate it to deployment duration or because the studied sample was not the target population of the present study. Studies have shown that a longer deployment time is associated with increased incidence of mental illness. Our analysis of the 13 identified studies indicated the existence of an association between exposure to deployment and mental illness onset. Conclusion: These findings will be useful to inform and guide future studies conducted in Brazil and worldwide
Studies on the Restriction of Murine Leukemia Viruses by Mouse APOBEC3
APOBEC3 proteins function to restrict the replication of retroviruses. One mechanism of this restriction is deamination of cytidines to uridines in (−) strand DNA, resulting in hypermutation of guanosines to adenosines in viral (+) strands. However, Moloney murine leukemia virus (MoMLV) is partially resistant to restriction by mouse APOBEC3 (mA3) and virtually completely resistant to mA3-induced hypermutation. In contrast, the sequences of MLV genomes that are in mouse DNA suggest that they were susceptible to mA3-induced deamination when they infected the mouse germline. We tested the possibility that sensitivity to mA3 restriction and to deamination resides in the viral gag gene. We generated a chimeric MLV in which the gag gene was from an endogenous MLV in the mouse germline, while the remainder of the viral genome was from MoMLV. This chimera was fully infectious but its response to mA3 was indistinguishable from that of MoMLV. Thus, the Gag protein does not seem to control the sensitivity of MLVs to mA3. We also found that MLVs inactivated by mA3 do not synthesize viral DNA upon infection; thus mA3 restriction of MLV occurs before or at reverse transcription. In contrast, HIV-1 restricted by mA3 and MLVs restricted by human APOBEC3G do synthesize DNA; these DNAs exhibit APOBEC3-induced hypermutation
Fluids in cosmology
We review the role of fluids in cosmology by first introducing them in
General Relativity and then by applying them to a FRW Universe's model. We
describe how relativistic and non-relativistic components evolve in the
background dynamics. We also introduce scalar fields to show that they are able
to yield an inflationary dynamics at very early times (inflation) and late
times (quintessence). Then, we proceed to study the thermodynamical properties
of the fluids and, lastly, its perturbed kinematics. We make emphasis in the
constrictions of parameters by recent cosmological probes.Comment: 34 pages, 4 figures, version accepted as invited review to the book
"Computational and Experimental Fluid Mechanics with Applications to Physics,
Engineering and the Environment". Version 2: typos corrected and references
expande
Two Genetic Determinants Acquired Late in Mus Evolution Regulate the Inclusion of Exon 5, which Alters Mouse APOBEC3 Translation Efficiency
Mouse apolipoprotein B mRNA-editing enzyme catalytic polypeptide-like editing complex 3 (mA3), an intracellular antiviral factor, has 2 allelic variations that are linked with different susceptibilities to beta- and gammaretrovirus infections among various mouse strains. In virus-resistant C57BL/6 (B6) mice, mA3 transcripts are more abundant than those in susceptible BALB/c mice both in the spleen and bone marrow. These strains of mice also express mA3 transcripts with different splicing patterns: B6 mice preferentially express exon 5-deficient (Δ5) mA3 mRNA, while BALB/c mice produce exon 5-containing full-length mA3 mRNA as the major transcript. Although the protein product of the Δ5 mRNA exerts stronger antiretroviral activities than the full-length protein, how exon 5 affects mA3 antiviral activity, as well as the genetic mechanisms regulating exon 5 inclusion into the mA3 transcripts, remains largely uncharacterized. Here we show that mA3 exon 5 is indeed a functional element that influences protein synthesis at a post-transcriptional level. We further employed in vitro splicing assays using genomic DNA clones to identify two critical polymorphisms affecting the inclusion of exon 5 into mA3 transcripts: the number of TCCT repeats upstream of exon 5 and the single nucleotide polymorphism within exon 5 located 12 bases upstream of the exon 5/intron 5 boundary. Distribution of the above polymorphisms among different Mus species indicates that the inclusion of exon 5 into mA3 mRNA is a relatively recent event in the evolution of mice. The widespread geographic distribution of this exon 5-including genetic variant suggests that in some Mus populations the cost of maintaining an effective but mutagenic enzyme may outweigh its antiviral function
The Confrontation between General Relativity and Experiment
The status of experimental tests of general relativity and of theoretical
frameworks for analysing them is reviewed. Einstein's equivalence principle
(EEP) is well supported by experiments such as the Eotvos experiment, tests of
special relativity, and the gravitational redshift experiment. Future tests of
EEP and of the inverse square law are searching for new interactions arising
from unification or quantum gravity. Tests of general relativity at the
post-Newtonian level have reached high precision, including the light
deflection, the Shapiro time delay, the perihelion advance of Mercury, and the
Nordtvedt effect in lunar motion. Gravitational-wave damping has been detected
in an amount that agrees with general relativity to better than half a percent
using the Hulse-Taylor binary pulsar, and other binary pulsar systems have
yielded other tests, especially of strong-field effects. When direct
observation of gravitational radiation from astrophysical sources begins, new
tests of general relativity will be possible.Comment: 89 pages, 8 figures; an update of the Living Review article
originally published in 2001; final published version incorporating referees'
suggestion
Different Modes of Retrovirus Restriction by Human APOBEC3A and APOBEC3G In Vivo
The apolipoprotein B editing complex 3 (A3) cytidine deaminases are among the most highly evolutionarily selected retroviral restriction factors, both in terms of gene copy number and sequence diversity. Primate genomes encode seven A3 genes, and while A3F and 3G are widely recognized as important in the restriction of HIV, the role of the other genes, particularly A3A, is not as clear. Indeed, since human cells can express multiple A3 genes, and because of the lack of an experimentally tractable model, it is difficult to dissect the individual contribution of each gene to virus restriction in vivo. To overcome this problem, we generated human A3A and A3G transgenic mice on a mouse A3 knockout background. Using these mice, we demonstrate that both A3A and A3G restrict infection by murine retroviruses but by different mechanisms: A3G was packaged into virions and caused extensive deamination of the retrovirus genomes while A3A was not packaged and instead restricted infection when expressed in target cells. Additionally, we show that a murine leukemia virus engineered to express HIV Vif overcame the A3G-mediated restriction, thereby creating a novel model for studying the interaction between these proteins. We have thus developed an in vivo system for understanding how human A3 proteins use different modes of restriction, as well as a means for testing therapies that disrupt HIV Vif-A3G interactions.United States. Public Health Service (Grant R01-AI-085015)United States. Public Health Service (Grant T32-CA115299 )United States. Public Health Service (Grant F32-AI100512
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