Crustal structure and rift flank uplift of the Adare Trough, Antarctica

The Adare Trough, located 100 km northeast of Cape Adare, Antarctica, represents the extinct third arm of a Tertiary spreading ridge between East and West Antarctica. It is characterized by pronounced asymmetric rift flanks elevated up to over 2 km above the trough's basement, accompanied by a large positive mantle Bouguer anomaly. On the basis of recently acquired seismic reflection and ship gravity data, we invert mantle Bouguer anomalies from the Adare Trough and obtain an unexpectedly large oceanic crustal thickness maximum of 9–10.5 km underneath the extinct ridge. A regional positive residual basement depth anomaly between 1 and 2.5 km in amplitude characterizes ocean crust from offshore Victoria Land to the Balleny Islands and north of Iselin Bank. The observations and models indicate that the mid/late Tertiary episode of slow spreading between East and West Antarctica was associated with a mantle thermal anomaly. The increasing crustal thickness toward the extinct ridge indicates that this thermal mantle anomaly may have increased in amplitude through time during the Adare spreading episode. This scenario is supported by a mantle convection model, which indicates the formation and strengthening of a major regional negative upper mantle density anomaly in the southwest Pacific in the last 50 million years. The total amount of post-26 Ma extension associated with Adare Trough normal faulting was about 7.5 km, in anomalously thick oceanic crust with a lithospheric effective elastic thickness (EET) between 3.5 and 5 km. This corresponds to an age between 3 and 5 million years based on a thermal boundary layer model and supports a scenario in which the Adare Trough formed soon after spreading between East and West Antarctica ceased, confined to relatively weak lithosphere with anomalously thick oceanic crust. There is little evidence for major subsequent structural activity in the Adare trough area from the available seismic data, indicating that this part of the West Antarctic Rift system became largely inactive in the early Miocene, with the exception of minor structural reactivation which is visible in the seismic data as offsets up to end of the early Pliocene

Resolution of tomographic models of the mantle beneath Iceland

The locations of volcanic islands may be controlled by thin or extending parts of the lithosphere over a partially molten asthenosphere [Anderson and Bass, 1984; Favela and Anderson, 2000], by edge effects near the boundaries of thick cratonic lithosphere [Anderson, 1998], or by narrow jets of hot mantle rising from deep within the mantle [Campbell and Griffiths, 1992; Morgan, 1971; Wilson, 1986]. Many hotspots are found on or near ridges, at lithospheric discontinuities, or in extensional environments, so high resolution seismic images are required to determine whether it is lithospheric structure, stresses in the lithosphere, or the deep mantle that is the controlling factor for the location of these volcanoes. In this study, we perform a simple experiment in which we use basic geometrical arguments to better understand the resolution of tomographic images of the upper 400 km of the mantle under Iceland. Our results indicate that a narrow, deep seated mantle plume is not required in order to explain the observed travel time delays in this region. Results of tomographic inversions are often viewed as unique; however, recent seismic studies of the Icelandic Hotspot have illustrated the non‐unique nature of these model

Data-Driven Homologue Matching for Chromosome Identification

Karyotyping involves the visualization and classification of chromosomes into standard classes. In normal human metaphase spreads, chromosomes occur in homologous pairs for the autosomal classes 1-22, and X chromosome for females. Many existing approaches for performing automated human chromosome image analysis presuppose cell normalcy, containing 46 chromosomes within a metaphase spread with two chromosomes per class. This is an acceptable assumption for routine automated chromosome image analysis. However, many genetic abnormalities are directly linked to structural or numerical aberrations of chromosomes within the metaphase spread. Thus, two chromosomes per class cannot be assumed for anomaly analysis. This paper presents the development of image analysis techniques which are extendible to detecting numerical aberrations evolving from structural abnormalities. Specifically, an approach to identifying normal chromosomes from selected class(es) within a metaphase spread is presented. Chromosome assignment to a specific class is initially based on neural networks, followed by banding pattern and centromeric index criteria checking, and concluding with homologue matching. Experimental results are presented comparing neural networks as the sole classifier to the authors\u27 homologue matcher for identifying class 17 within normal and abnormal metaphase spreads

Abnormal Cell Detection using the Choquet Integral

Automated Giemsa-banded chromosome image research has been largely restricted to classification schemes associated with isolated chromosomes within metaphase spreads. In normal human metaphase spreads, there are 46 chromosomes occurring in homologous pairs for the autosomal classes 1-22 and the X chromosome for females. Many genetic abnormalities are directly linked to structural and/or numerical aberrations of chromosomes within metaphase spreads. Cells with the Philadelphia chromosome contain an abnormal chromosome for class 9 and for class 22, leaving a single normal chromosome for each class. A data-driven homologue matching technique is applied to recognizing normal chromosomes from classes 9 and 22. Homologue matching integrates neural networks, dynamic programming and the Choquet integral for chromosome recognition. The inability to locate matching homologous pairs for classes 9 and 22 provides an indication that the cell is abnormal, potentially containing the Philadelphia chromosome. Applying this technique to 50 normal and to 48 abnormal cells containing the Philadelphia chromosome yields 100.0% correct abnormal cell detection with a 24.0% false positive rate

From Parasite to Mutualist: Rapid Evolution of Wolbachia in Natural Populations of Drosophila

Wolbachia are maternally inherited bacteria that commonly spread through host populations by causing cytoplasmic incompatibility, often expressed as reduced egg hatch when uninfected females mate with infected males. Infected females are frequently less fecund as a consequence of Wolbachia infection. However, theory predicts that because of maternal transmission, these “parasites” will tend to evolve towards a more mutualistic association with their hosts. Drosophila simulans in California provided the classic case of a Wolbachia infection spreading in nature. Cytoplasmic incompatibility allowed the infection to spread through individual populations within a few years and from southern to northern California (more than 700 km) within a decade, despite reducing the fecundity of infected females by 15%–20% under laboratory conditions. Here we show that the Wolbachia in California D. simulans have changed over the last 20 y so that infected females now exhibit an average 10% fecundity advantage over uninfected females in the laboratory. Our data suggest smaller but qualitatively similar changes in relative fecundity in nature and demonstrate that fecundity-increasing Wolbachia variants are currently polymorphic in natural populations

Snapshots of a protein folding intermediate

We have investigated the folding dynamics of Thermus thermophilus cytochrome c_(552) by time-resolved fluorescence energy transfer between the heme and each of seven site-specific fluorescent probes. We have found both an equilibrium unfolding intermediate and a distinct refolding intermediate from kinetics studies. Depending on the protein region monitored, we observed either two-state or three-state denaturation transitions. The unfolding intermediate associated with three-state folding exhibited native contacts in β-sheet and C-terminal helix regions. We probed the formation of a refolding intermediate by time-resolved fluorescence energy transfer between residue 110 and the heme using a continuous flow mixer. The intermediate ensemble, a heterogeneous mixture of compact and extended polypeptides, forms in a millisecond, substantially slower than the ∼100-μs formation of a burst-phase intermediate in cytochrome c. The surprising finding is that, unlike for cytochrome c, there is an observable folding intermediate, but no microsecond burst phase in the folding kinetics of the structurally related thermostable protein

First Science Observations with SOFIA/FORCAST: Properties of Intermediate-Luminosity Protostars and Circumstellar Disks in OMC-2

We examine eight young stellar objects in the OMC-2 star forming region based on observations from the SOFIA/FORCAST early science phase, the Spitzer Space Telescope, the Herschel Space Observatory, 2MASS, APEX, and other results in the literature. We show the spectral energy distributions of these objects from near-infrared to millimeter wavelengths, and compare the SEDs with those of sheet collapse models of protostars and circumstellar disks. Four of the objects can be modelled as protostars with infalling envelopes, two as young stars surrounded by disks, and the remaining two objects have double-peaked SEDs. We model the double-peaked sources as binaries containing a young star with a disk and a protostar. The six most luminous sources are found in a dense group within a 0.15 x 0.25 pc region; these sources have luminosities ranging from 300 L_sun to 20 L_sun. The most embedded source (OMC-2 FIR 4) can be fit by a class 0 protostar model having a luminosity of ~50 L_sun and mass infall rate of ~10^-4 solar masses per year.Comment: Accepted by ApJ Letter

The timing and location of glial cell line-derived neurotrophic factor expression determine enteric nervous system structure and function

Ret signaling is critical for formation of the enteric nervous system (ENS) because Ret activation promotes ENS precursor survival, proliferation, and migration and provides trophic support for mature enteric neurons. While these roles are well established, we now provide evidence that increasing levels of the Ret ligand GDNF in mice causes alterations in ENS structure and function that are critically dependent on the time and location of increased GDNF availability. This is demonstrated using two different strains of transgenic mice and by injecting newborn mice with GDNF. Furthermore, because different subclasses of ENS precursors withdraw from the cell cycle at different times during development, increases in GDNF at specific times alter the ratio of neuronal subclasses in the mature ENS. In addition, we confirm that esophageal neurons are GDNF responsive and demonstrate that the location of GDNF production influences neuronal process projection for NADPH diaphorase expressing, but not acetylcholinesterase, choline acetyltransferase, or tryptophan hydroxylase expressing small bowel myenteric neurons. We further demonstrate that changes in GDNF availability influence intestinal function in vitro and in vivo. Thus, changes in GDNF expression can create a wide variety of alterations in ENS structure and function and may in part contribute to human motility disorders

Surfactant status and respiratory outcome in premature infants receiving late surfactant treatment.

BACKGROUND:Many premature infants with respiratory failure are deficient in surfactant, but the relationship to occurrence of bronchopulmonary dysplasia (BPD) is uncertain. METHODS:Tracheal aspirates were collected from 209 treated and control infants enrolled at 7-14 days in the Trial of Late Surfactant. The content of phospholipid, surfactant protein B, and total protein were determined in large aggregate (active) surfactant. RESULTS:At 24 h, surfactant treatment transiently increased surfactant protein B content (70%, p < 0.01), but did not affect recovered airway surfactant or total protein/phospholipid. The level of recovered surfactant during dosing was directly associated with content of surfactant protein B (r = 0.50, p < 0.00001) and inversely related to total protein (r = 0.39, p < 0.0001). For all infants, occurrence of BPD was associated with lower levels of recovered large aggregate surfactant, higher protein content, and lower SP-B levels. Tracheal aspirates with lower amounts of recovered surfactant had an increased proportion of small vesicle (inactive) surfactant. CONCLUSIONS:We conclude that many intubated premature infants are deficient in active surfactant, in part due to increased intra-alveolar metabolism, low SP-B content, and protein inhibition, and that the severity of this deficit is predictive of BPD. Late surfactant treatment at the frequency used did not provide a sustained increase in airway surfactant