267 research outputs found

    Simulations of Gaseous Disc-Embedded Planet Interaction

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    We present three-dimensional self-gravitating smoothed-particle hydrodynamics (SPH) simulations of an isothermal gaseous disc interacting with an embedded planet. Discs of varying stability are simulated with planets ranging from 10 Earth-masses to 2 Jupiter-masses. The SPH technique provides the large dynamic range needed to accurately capture the large scale behavior of the disc as well as the small scale interaction of the planet with surrounding material. Most runs used 10^5 gas particles, giving us the spatial resolution required to observe the formation of planets. We find four regions in parameter space: low-mass planets undergo Type I migration; higher-mass planets can form a gap; the gravitational instability mode of planet formation in marginally stable discs can be triggered by embedded planets; discs that are completely unstable can fragment to form many planets. The disc stability is the most important factor in determing which interaction a system will exhibit. For the stable disc cases, our migration and accretion time-scales are shorter and scale differently than previously suggested.Comment: 10 pages, 8 figures, see http://hpcc.astro.washington.edu/grads/gwl/disc_planet_interaction for high-resolution color figures and movie

    Time-Dependence of the Mass Accretion Rate in Cluster Cooling Flows

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    We analyze two time-dependent cluster cooling flow models in spherical symmetry. The first assumes that the intracluster gas resides in a static external potential, and includes the effects of optically thin radiative cooling and mass deposition. This corresponds to previous steady-state cooling flow models calculated by White & Sarazin (1987). Detailed agreement is found between steady-state models and time-dependent models at fixed times in the simulations. The mass accretion rate is found either to increase or remain nearly constant once flows reach a steady state. The time rate of change of the accretion rate is strongly sensitive to the value of the mass deposition parameter q, but only mildly sensitive to the ratio beta of gravitational binding energy to gas temperature. We show that previous scaling arguments presented by Bertschinger (1988) and White (1988) are valid only for mature cooling flows with weak mass deposition (q ~< 1). The second set of models includes the effects of a secularly deepening cluster potential and secondary infall of gas from the Hubble flow. We find that such heating effects do not prevent the flows from reaching a steady state within an initial central cooling time.Comment: 22 pages (AASTeX) with 16 EPS figures; accepted for publication in The Astrophysical Journa

    The Interaction of 3C401 with the Surrounding Intracluster Medium

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    We present an observation of the radio-galaxy 3C401 and the surrounding intracluster medium (ICM) of its host galaxy cluster by the Chandra X-ray Observatory. This luminous radio-galaxy is notable in that it has characteristics intermediate between the FRI and FRII morphologies. We clearly detect point-like emission coincident with the radio-core of 3C401, although the spatial resolution of even Chandra is only 2kpc at the distance of 3C401 (z=0.201) and so the possibility remains that this is a dense (and rapidly cooling) thermal gaseous core in the center of the ICM atmosphere. Strong departures from spherical symmetry in the central 10-20kpc of the ICM clearly suggest interaction between the ICM and the radio-lobes of 3C401. A central X-ray bar probably results from the evacuation of two ICM cavities by the expanding radio lobes. Beyond these central regions, the cluster possesses a flatter profile than many clusters of comparable mass suggesting the importance of ICM heating and entropy injection by 3C401. We detect an interesting cross-like structure in the ICM on 100kpc scales. We speculate that this could be a radio-galaxy induced disturbance corresponding to a time when 3C401 was substantially more powerful. A particularly exciting possibility is that this cross-like structure corresponds to a large scale global g-mode oscillation excited by a past outburst of 3C401.Comment: 7 pages, 5 postscript figures. Accepted for publication in MNRA

    Transcriptome Analysis of Zebrafish Embryogenesis Using Microarrays

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    Zebrafish (Danio rerio) is a well-recognized model for the study of vertebrate developmental genetics, yet at the same time little is known about the transcriptional events that underlie zebrafish embryogenesis. Here we have employed microarray analysis to study the temporal activity of developmentally regulated genes during zebrafish embryogenesis. Transcriptome analysis at 12 different embryonic time points covering five different developmental stages (maternal, blastula, gastrula, segmentation, and pharyngula) revealed a highly dynamic transcriptional profile. Hierarchical clustering, stage-specific clustering, and algorithms to detect onset and peak of gene expression revealed clearly demarcated transcript clusters with maximum gene activity at distinct developmental stages as well as co-regulated expression of gene groups involved in dedicated functions such as organogenesis. Our study also revealed a previously unidentified cohort of genes that are transcribed prior to the mid-blastula transition, a time point earlier than when the zygotic genome was traditionally thought to become active. Here we provide, for the first time to our knowledge, a comprehensive list of developmentally regulated zebrafish genes and their expression profiles during embryogenesis, including novel information on the temporal expression of several thousand previously uncharacterized genes. The expression data generated from this study are accessible to all interested scientists from our institute resource database (http://giscompute.gis.a-star.edu.sg/~govind/zebrafish/data_download.html)

    Mice with targeted disruptions in the paralogous genes hoxa-3 and hoxd-3 reveal synergistic interactions.

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    Journal ArticleThe Hox genes encode transcription factors which mediate the formation of the mammalian body plan along the anteroposterior and appendicular axes. Paralogous Hox genes within the separate linkage groups are closely related with respect to DNA sequence and expression, suggesting that they could have at least partially redundant functions. We showed previously that mice homozygous for independent targeted disruptions in the paralogous genes hoxa-3 and hoxd-3 had no defects in common. But our current analysis of double mutants has revealed strong, dosage-dependent interactions between these genes. We report here that in hoxd-3- homozygotes the first cervical vertebra, the atlas, is homeotically transformed to the adjacent anterior structure. Unexpectedly, in double mutants, rather than observing a more extensive homeotic transformation, the entire atlas is deleted. These observations are interpreted in terms of a model in which these Hox genes differentially regulate the proliferation rates of the appropriate sets of precursor cells

    The relationship of systemic markers of renal function and vascular function with retinal blood vessel responses

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    Purpose: To test the hypothesis of a significant relationship between systemic markers of renal and vascular function (processes linked to cardiovascular disease and its development) and retinal microvascular function in diabetes and/or cardiovascular disease.Methods: Ocular microcirculatory function was measured in 116 patients with diabetes and/or cardiovascular disease using static and continuous retinal vessel responses to three cycles of flickering light. Endothelial function was evaluated by von Willebrand factor (vWf), endothelial microparticles and soluble E selectin, renal function by serum creatinine, creatinine clearance and estimated glomerular filtration rate (eGFR). HbA1c was used as a control index.Results: Central retinal vein equivalence and venous maximum dilation to flicker were linked to HbA1c (both p<0.05). Arterial reaction time was linked to serum creatinine (p=0.036) and eGFR (p=0.039), venous reaction time was linked to creatinine clearance (p=0.018). Creatinine clearance and eGFR were linked to arterial maximum dilatation (p<0.001 and p=0.003 respectively) and the dilatation amplitude (p=0.038 and p=0.048 respectively) responses in the third flicker cycle. Of venous responses to the first flicker cycle, HbA1c was linked to the maximum dilation response (p=0.004) and dilatation amplitude (p=0.017), vWf was linked to the maximum constriction response (p=0.016), and creatinine clearance to the baseline diameter fluctuation (p=0.029). In the second flicker cycle, dilatation amplitude was linked to serum creatinine (p=0.022). Conclusions: Several retinal blood vessel responses to flickering light are linked to glycaemia and renal function, but only one index is linked to endothelial function. Renal function must be considered when interpreting retinal vessel responses

    Deletion of the WD40 Domain of LRRK2 in Zebrafish Causes Parkinsonism-Like Loss of Neurons and Locomotive Defect

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    LRRK2 plays an important role in Parkinson's disease (PD), but its biological functions are largely unknown. Here, we cloned the homolog of human LRRK2, characterized its expression, and investigated its biological functions in zebrafish. The blockage of zebrafish LRRK2 (zLRRK2) protein by morpholinos caused embryonic lethality and severe developmental defects such as growth retardation and loss of neurons. In contrast, the deletion of the WD40 domain of zLRRK2 by morpholinos targeting splicing did not induce severe embryonic developmental defects; rather it caused Parkinsonism-like phenotypes, including loss of dopaminergic neurons in diencephalon and locomotion defects. These neurodegenerative and locomotion defects could be rescued by over-expressing zLRRK2 or hLRRK2 mRNA. The administration of L-dopa could also rescue the locomotion defects, but not the neurodegeneration. Taken together, our results demonstrate that zLRRK2 is an ortholog of hLRRK2 and that the deletion of WD40 domain of zLRRK2 provides a disease model for PD
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