200 research outputs found
The transmission spectrum of Earth through lunar eclipse observations
Of the 342 planets discovered so far orbiting other stars, 58 "transit" the
stellar disk, meaning that they can be detected by a periodic decrease in the
starlight flux. The light from the star passes through the atmosphere of the
planet, and in a few cases the basic atmospheric composition of the planet can
be estimated. As we get closer to finding analogues of Earth, an important
consideration toward the characterization of exoplanetary atmospheres is what
the transmission spectrum of our planet looks like. Here we report the optical
and near-infrared transmission spectrum of the Earth, obtained during a lunar
eclipse. Some biologically relevant atmospheric features that are weak in the
reflected spectrum (such as ozone, molecular oxygen, water, carbon dioxide and
methane) are much stronger in the transmission spectrum, and indeed stronger
than predicted by modelling. We also find the fingerprints of the Earth's
ionosphere and of the major atmospheric constituent, diatomic nitrogen (N2),
which are missing in the reflected spectrum.Comment: Published in Nature, 11 July 2009. This file also contains the
on-line materia
Massive star formation in 100,000 years from turbulent and pressurized molecular clouds
Massive stars (with mass m_* > 8 solar masses) are fundamental to the
evolution of galaxies, because they produce heavy elements, inject energy into
the interstellar medium, and possibly regulate the star formation rate. The
individual star formation time, t_*f, determines the accretion rate of the
star; the value of the former quantity is currently uncertain by many orders of
magnitude, leading to other astrophysical questions. For example, the variation
of t_*f with stellar mass dictates whether massive stars can form
simultaneously with low-mass stars in clusters. Here we show that t_*f is
determined by conditions in the star's natal cloud, and is typically ~10^5 yr.
The corresponding mass accretion rate depends on the pressure within the cloud
- which we relate to the gas surface density - and on both the instantaneous
and final stellar masses. Characteristic accretion rates are sufficient to
overcome radiation pressure from ~100 solar mass protostars, while
simultaneously driving intense bipolar gas outflows. The weak dependence of
t_*f on the final mass of the star allows high- and low-mass star formation to
occur nearly simultaneously in clusters.Comment: 9 pages plus 2 figures, Nature, 416, 59 (7th March 2002
‘This constant being woken up is the worst thing’ – experiences of sleep in fibromyalgia syndrome
Runx1 Loss Minimally Impacts Long-Term Hematopoietic Stem Cells
RUNX1 encodes a DNA binding subunit of the core-binding transcription factors and is frequently mutated in acute leukemia, therapy-related leukemia, myelodysplastic syndrome, and chronic myelomonocytic leukemia. Mutations in RUNX1 are thought to confer upon hematopoietic stem cells (HSCs) a pre-leukemic state, but the fundamental properties of Runx1 deficient pre-leukemic HSCs are not well defined. Here we show that Runx1 deficiency decreases both apoptosis and proliferation, but only minimally impacts the frequency of long term repopulating HSCs (LT-HSCs). It has been variously reported that Runx1 loss increases LT-HSC numbers, decreases LT-HSC numbers, or causes age-related HSC exhaustion. We attempt to resolve these discrepancies by showing that Runx1 deficiency alters the expression of several key HSC markers, and that the number of functional LT-HSCs varies depending on the criteria used to score them. Finally, we identify genes and pathways, including the cell cycle and p53 pathways that are dysregulated in Runx1 deficient HSCs
Gaze following is modulated by expectations regarding others’ action goals
Humans attend to social cues in order to understand and predict others' behavior. Facial expressions and gaze direction provide valuable information to infer others' mental states and intentions. The present study examined the mechanism of gaze following in the context of participants' expectations about successive action steps of an observed actor. We embedded a gaze-cueing manipulation within an action scenario consisting of a sequence of naturalistic photographs. Gaze-induced orienting of attention (gaze following) was analyzed with respect to whether the gaze behavior of the observed actor was in line or not with the action-related expectations of participants (i.e., whether the actor gazed at an object that was congruent or incongruent with an overarching action goal). In Experiment 1, participants followed the gaze of the observed agent, though the gaze-cueing effect was larger when the actor looked at an action-congruent object relative to an incongruent object. Experiment 2 examined whether the pattern of effects observed in Experiment 1 was due to covert, rather than overt, attentional orienting, by requiring participants to maintain eye fixation throughout the sequence of critical photographs (corroborated by monitoring eye movements). The essential pattern of results of Experiment 1 was replicated, with the gaze-cueing effect being completely eliminated when the observed agent gazed at an action-incongruent object. Thus, our findings show that covert gaze following can be modulated by expectations that humans hold regarding successive steps of the action performed by an observed agent
Induction of B-cell lymphoma by UVB Radiation in p53 Haploinsufficient Mice
<p>Abstract</p> <p>Background</p> <p>The incidence of non-Hodgkin's lymphoma has increased over recent years. The exact etiology of lymphoma remains unknown. Ultraviolet light exposure has been associated with the development of internal lymphoid malignancies and some reports suggest that it may play a role in the development of lymphoma in humans. Here we describe the characterization and progression of lymphoma in p53 heterozygous mice exposed to UVB irradiation.</p> <p>Methods</p> <p>UVB-irradiated p53<sup>+/- </sup>mice developed enlargement of the spleen. Isolated spleen cells were transplanted into Rag deficient hosts. The UV-induced tumor cells were analyzed by flow cytometry. The tumor cells were tagged with GFP to study their metastatic potential. SKY and karyotypic analysis were carried out for the detection of chromosomal abnormalities. Functional assays included in vitro class switch recombination assay, immunoglobulin rearrangement assay, as well as cytokine profiling.</p> <p>Results</p> <p>UVB-exposed mice showed enlargement of the spleen and lymph nodes. Cells transplanted into Rag deficient mice developed aggressive tumors that infiltrated the lymph nodes, the spleen and the bone marrow. The tumor cells did not grow in immune competent syngeneic C57Bl/6 mice yet showed a modest growth in UV-irradiated B6 mice. Phenotypic analysis of these tumor cells revealed these cells are positive for B cell markers CD19<sup>+</sup>, CD5<sup>+</sup>, B220<sup>+</sup>, IgM<sup>+ </sup>and negative for T cell, NK or dendritic cell markers. The UV-induced tumor cells underwent robust in vitro immunoglobulin class switch recombination in response to lipopolysaccharide. Cytogenetic analysis revealed a t(14;19) translocation and trisomy of chromosome 6. These tumor cells secret IL-10, which can promote tumor growth and cause systemic immunosuppression.</p> <p>Conclusion</p> <p>UV-irradiated p53<sup>+/- </sup>mice developed lymphoid tumors that corresponded to a mature B cell lymphoma. Our results suggest that an indirect mechanism is involved in the development of internal tumors after chronic exposure to UV light. The induction of B cell lymphoma in UV-irradiated p53 heterozygous mice may provide a useful model for lymphoma development in humans.</p
Early over expression of messenger RNA for multiple genes, including insulin, in the Pancreatic Lymph Nodes of NOD mice is associated with Islet Autoimmunity
<p>Abstract</p> <p>Background</p> <p>Autoimmune diabetes (T1D) onset is preceded by a long inflammatory process directed against the insulin-secreting β cells of the pancreas. Deciphering the early autoimmune mechanisms represents a challenge due to the absence of clinical signs at early disease stages. The aim of this study was to identify genes implicated in the early steps of the autoimmune process, prior to inflammation, in T1D. We have previously established that insulin autoantibodies (E-IAA) predict early diabetes onset delineating an early phenotypic check point (window 1) in disease pathogenesis. We used this sub-phenotype and applied differential gene expression analysis in the pancreatic lymph nodes (PLN) of 5 weeks old Non Obese Diabetic (NOD) mice differing solely upon the presence or absence of E-IAA. Analysis of gene expression profiles has the potential to provide a global understanding of the disease and to generate novel hypothesis concerning the initiation of the autoimmune process.</p> <p>Methods</p> <p>Animals have been screened weekly for the presence of E-IAA between 3 and 5 weeks of age. E-IAA positive or negative NOD mice at least twice were selected and RNAs isolated from the PLN were used for microarray analysis. Comparison of transcriptional profiles between positive and negative animals and functional annotations of the resulting differentially expressed genes, using software together with manual literature data mining, have been performed.</p> <p>Results</p> <p>The expression of 165 genes was modulated between E-IAA positive and negative PLN. In particular, genes coding for insulin and for proteins known to be implicated in tissue remodelling and Th1 immunity have been found to be highly differentially expressed. Forty one genes showed over 5 fold differences between the two sets of samples and 30 code for extracellular proteins. This class of proteins represents potential diagnostic markers and drug targets for T1D.</p> <p>Conclusion</p> <p>Our data strongly suggest that the immune related mechanisms taking place at this early age in the PLN, correlate with homeostatic changes influencing tissue integrity of the adjacent pancreatic tissue. Functional analysis of the identified genes suggested that similar mechanisms might be operating during pre-inflammatory processes deployed in tissues i) hosting parasitic microorganisms and ii) experiencing unrestricted invasion by tumour cells.</p
Trypanosoma vivax Infections: Pushing Ahead with Mouse Models for the Study of Nagana. II. Immunobiological Dysfunctions
Trypanosoma vivax is the main species involved in trypanosomosis, but very little is known about the immunobiology of the infective process caused by this parasite. Recently we undertook to further characterize the main parasitological, haematological and pathological characteristics of mouse models of T. vivax infection and noted severe anemia and thrombocytopenia coincident with rising parasitemia. To gain more insight into the organism's immunobiology, we studied lymphocyte populations in central (bone marrow) and peripherical (spleen and blood) tissues following mouse infection with T. vivax and showed that the immune system apparatus is affected both quantitatively and qualitatively. More precisely, after an initial increase that primarily involves CD4+ T cells and macrophages, the number of splenic B cells decreases in a step-wise manner. Our results show that while infection triggers the activation and proliferation of Hematopoietic Stem Cells, Granulocyte-Monocyte, Common Myeloid and Megacaryocyte Erythrocyte progenitors decrease in number in the course of the infection. An in-depth analysis of B-cell progenitors also indicated that maturation of pro-B into pre-B precursors seems to be compromised. This interferes with the mature B cell dynamics and renewal in the periphery. Altogether, our results show that T. vivax induces profound immunological alterations in myeloid and lymphoid progenitors which may prevent adequate control of T. vivax trypanosomosis
Efficacy of high-intensity, low-volume interval training compared to continuous aerobic training on insulin resistance, skeletal muscle structure and function in adults with metabolic syndrome: study protocol for a randomized controlled clinical trial (Intraining-MET)
ABSTRACT: Evidence of the efficacy of high-intensity, low-volume interval training (HIIT-low volume) in treating insulin resistance (IR) in patients with metabolic disorders is contradictory. In addition, it is unknown whether this effect is mediated through muscle endocrine function, which in turn depends on muscle mass and fiber type composition. Our aims were to assess the efficacy of HIIT-low volume compared to continuous aerobic exercise (CAE) in treating IR in adults with metabolic syndrome (MS) and to establish whether musclin, apelin, muscle mass and muscle composition are mediators of the effect. Methods: This is a controlled, randomized, clinical trial using the minimization method, with blinding of those who will evaluate the outcomes and two parallel groups for the purpose of showing superiority. Sixty patients with MS and IR with ages between 40 and 60 years will be included. A clinical evaluation will be carried out, along with laboratory tests to evaluate IR (homeostatic model assessment (HOMA)), muscle endocrine function (serum levels of musclin and apelin), thigh muscle mass (by dual energy x-ray absorptiometry (DXA) and thigh muscle composition (by carnosine measurement with proton magnetic resonance spectroscopy (H–MRS)), before and after 12 weeks of a treadmill exercise program three times a week. Participants assigned to the intervention (n = 30) will receive HIIT-low volume in 22-min sessions that will include six intervals at a load of 90% of maximum oxygen consumption (VO2 max) for 1 min followed by 2 min at 50% of VO2 max. The control group (n = 30) will receive CAE at an intensity of 60% of VO2 max for 36 min. A theoretical model based on structural equations will be proposed to estimate the total, direct and indirect effects of training on IR and the proportion explained by the mediators. Discussion: Compared with CAE, HIIT-low volume can be effective and efficient at improving physical capacity and decreasing cardiovascular risk factors, such as IR, in patients with metabolic disorders. Studies that evaluate mediating variables of the effect of HIIT-low volume on IR, such as endocrine function and skeletal muscle structure, are necessary to understand the role of skeletal muscle in the pathophysiology of MS and their regulation by exercise. Trial registration: NCT03087721. High-intensity Interval, Low Volume Training in Metabolic Syndrome (Intraining-MET). Registered on 22 March 2017, retrospectively registered
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