Interferometric imaging of the sulfur-bearing molecules H2S, SO and CS in comet C/1995 O1 (Hale-Bopp)

We present observations of rotational lines of H2S, SO and CS performed in comet C/1995 O1 (Hale-Bopp) in March 1997 with the Plateau de Bure interferometer (IRAM). The observations provide informations on the spatial and velocity distributions of these molecules. They can be used to constrain their photodissociation rate and their origin. We use a radiative transfer code which allows us to compute synthetic line profiles and interferometric maps, to be compared to the observations. Both single-dish spectra and interferometric spectral maps show a day/night asymmetry in the outgassing. From the analysis of the spectral maps, including the astrometry, we show that SO and CS present in addition a jet-like structure that may be the gaseous counterpart of the dust high-latitude jet observed in optical images. A CS rotating jet is also observed. Using the astrometry provided by continuum radio maps obtained in parallel, we conclude that there is no need to invoke of nongravitational forces acting on this comet, and provide an updated orbit. The radial extension of H2S is found to be consistent with direct release from the nucleus. SO displays an extended radial distribution. Assuming that SO2 is the parent of SO, the photodissociation rate of SO is measured to be 1.5 E-4 s-1 at 1 AU from the Sun. This is lower than most laboratory-based estimates and may suggest that SO is not solely produced by SO2 photolysis. From the observations of J(2-1) and J(5-4) CS lines, we deduce a CS photodissociation rate of 1 to 5 E-5 s-1. The photodissociation rate of CS2, the likely parent of CS, cannot be constrained due to insufficient resolution, but our data are consistent with published values. These observations illustrate the cometary science that will be performed with the future ALMA interferometer.Comment: Accepted for publication in Astronomy & Astrophysic

Apaf-1 and caspase-9 accelerate apoptosis, but do not determine whether factor-deprived or drug-treated cells die

Apoptosis after growth factor withdrawal or drug treatment is associated with mitochondrial cytochrome c release and activation of Apaf-1 and caspase-9. To determine whether loss of Apaf-1, caspase-2, and caspase-9 prevented death of factor-starved cells, allowing them to proliferate when growth factor was returned, we generated IL-3–dependent myeloid lines from gene-deleted mice. Long after growth factor removal, cells lacking Apaf-1, caspase-9 or both caspase-9 and caspase-2 appeared healthy, retained intact plasma membranes, and did not expose phosphatidylserine. However, release of cytochrome c still occurred, and they failed to form clones when IL-3 was restored. Cells lacking caspase-2 alone had no survival advantage. Therefore, Apaf-1, caspase-2, and caspase-9 are not required for programmed cell death of factor-dependent cells, but merely affect its rate. In contrast, transfection with Bcl-2 provided long-term, clonogenic protection, and could act independently of the apoptosome. Unlike expression of Bcl-2, loss of Apaf-1, caspase-2, or caspase-9 would therefore be unlikely to enhance the survival of cancer cells

Self-consistent anisotropic oscillator with cranked angular and vortex velocities

The Kelvin circulation is the kinematical Hermitian observable that measures the true character of nuclear rotation. For the anisotropic oscillator, mean field solutions with fixed angular momentum and Kelvin circulation are derived in analytic form. The cranking Lagrange multipliers corresponding to the two constraints are the angular and vortex velocities. Self-consistent solutions are reported with a constraint to constant volume.Comment: 12 pages, LaTex/RevTex, Phys. Rev. C4

On the recurrence and robust properties of Lorenz'63 model

Lie-Poisson structure of the Lorenz'63 system gives a physical insight on its dynamical and statistical behavior considering the evolution of the associated Casimir functions. We study the invariant density and other recurrence features of a Markov expanding Lorenz-like map of the interval arising in the analysis of the predictability of the extreme values reached by particular physical observables evolving in time under the Lorenz'63 dynamics with the classical set of parameters. Moreover, we prove the statistical stability of such an invariant measure. This will allow us to further characterize the SRB measure of the system.Comment: 44 pages, 7 figures, revised version accepted for pubblicatio

Development of strategies to support home-based exercise adherence after stroke: a Delphi consensus

Objective To develop a set of strategies to enhance adherence to home-based exercises after stroke, and an overarching framework to classify these strategies. Method We conducted a four-round Delphi consensus (two online surveys, followed by a focus group then a consensus round). The Delphi panel consisted of 13 experts from physiotherapy, occupational therapy, clinical psychology, behaviour science and community medicine. The experts were from India, Australia and UK. Results In round 1, a 10-item survey using open-ended questions was emailed to panel members and 75 strategies were generated. Of these, 25 strategies were included in round 2 for further consideration. A total of 64 strategies were finally included in the subsequent rounds. In round 3, the strategies were categorised into nine domains - (1) patient education on stroke and recovery, (2) method of exercise prescription, (3) feedback and supervision, (4) cognitive remediation, (5) involvement of family members, (6) involvement of society, (7) promoting self-efficacy, (8) motivational strategies and (9) reminder strategies. The consensus from 12 experts (93%) led to the development of the framework in round 4. Conclusion We developed a framework of comprehensive strategies to assist clinicians in supporting exercise adherence among stroke survivors. It provides practical methods that can be deployed in both research and clinical practices. Future studies should explore stakeholders' experiences and the cost-effectiveness of implementing these strategies

Alterations in the gut microbiome implicate key taxa and metabolic pathways across inflammatory arthritis phenotypes

Musculoskeletal diseases affect up to 20% of adults worldwide. The gut microbiome has been implicated in inflammatory conditions, but large-scale metagenomic evaluations have not yet traced the routes by which immunity in the gut affects inflammatory arthritis. To characterize the community structure and associated functional processes driving gut microbial involvement in arthritis, the Inflammatory Arthritis Microbiome Consortium investigated 440 stool shotgun metagenomes comprising 221 adults diagnosed with rheumatoid arthritis, ankylosing spondylitis, or psoriatic arthritis and 219 healthy controls and individuals with joint pain without an underlying inflammatory cause. Diagnosis explained about 2% of gut taxonomic variability, which is comparable in magnitude to inflammatory bowel disease. We identified several candidate microbes with differential carriage patterns in patients with elevated blood markers for inflammation. Our results confirm and extend previous findings of increased carriage of typically oral and inflammatory taxa and decreased abundance and prevalence of typical gut clades, indicating that distal inflammatory conditions, as well as local conditions, correspond to alterations to the gut microbial composition. We identified several differentially encoded pathways in the gut microbiome of patients with inflammatory arthritis, including changes in vitamin B salvage and biosynthesis and enrichment of iron sequestration. Although several of these changes characteristic of inflammation could have causal roles, we hypothesize that they are mainly positive feedback responses to changes in host physiology and immune homeostasis. By connecting taxonomic alternations to functional alterations, this work expands our understanding of the shifts in the gut ecosystem that occur in response to systemic inflammation during arthritis

Carbonylation of Csp3−H Bonds through Oxidative Wittig‐Type Reaction: An Unprecedented Version of Wittig Reaction

A Wittig‐type reaction was achieved by radical cation salt induced aerobic oxidation of Csp3−H bonds. Different from the “standard” version of the Wittig reaction, in which a carbon‐carbon double bond is formed from a carbonyl, carbonyl groups can be installed by similar process.Not from carbonyls but to carbonyls: A Wittig‐type reaction was achieved by radical cation salt induced aerobic oxidation of sp3 C−H bonds. Different from the “standard” version of the Wittig reaction, in which a carbon‐carbon double bond is formed from a carbonyl, carbonyl groups can be installed by similar process.Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/137437/1/ajoc201600055-sup-0001-misc_information.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/137437/2/ajoc201600055.pd

Alterations in the gut microbiome implicate key taxa and metabolic pathways across inflammatory arthritis phenotypes

Musculoskeletal diseases affect up to 20% of adults worldwide. The gut microbiome has been implicated in inflammatory conditions, but large-scale metagenomic evaluations have not yet traced the routes by which immunity in the gut affects inflammatory arthritis. To characterize the community structure and associated functional processes driving gut microbial involvement in arthritis, the Inflammatory Arthritis Microbiome Consortium investigated 440 stool shotgun metagenomes comprising 221 adults diagnosed with rheumatoid arthritis, ankylosing spondylitis, or psoriatic arthritis and 219 healthy controls and individuals with joint pain without an underlying inflammatory cause. Diagnosis explained about 2% of gut taxonomic variability, which is comparable in magnitude to inflammatory bowel disease. We identified several candidate microbes with differential carriage patterns in patients with elevated blood markers for inflammation. Our results confirm and extend previous findings of increased carriage of typically oral and inflammatory taxa and decreased abundance and prevalence of typical gut clades, indicating that distal inflammatory conditions, as well as local conditions, correspond to alterations to the gut microbial composition. We identified several differentially encoded pathways in the gut microbiome of patients with inflammatory arthritis, including changes in vitamin B salvage and biosynthesis and enrichment of iron sequestration. Although several of these changes characteristic of inflammation could have causal roles, we hypothesize that they are mainly positive feedback responses to changes in host physiology and immune homeostasis. By connecting taxonomic alternations to functional alterations, this work expands our understanding of the shifts in the gut ecosystem that occur in response to systemic inflammation during arthritis