A high signal to noise ratio map of the Sunyaev-Zel'dovich increment at 1.1 mm wavelength in Abell 1835

We present an analysis of an 8 arcminute diameter map of the area around the galaxy cluster Abell 1835 from jiggle map observations at a wavelength of 1.1 mm using the Bolometric Camera (Bolocam) mounted on the Caltech Submillimeter Observatory (CSO). The data is well described by a model including an extended Sunyaev-Zel'dovich (SZ) signal from the cluster gas plus emission from two bright background submm galaxies magnified by the gravitational lensing of the cluster. The best-fit values for the central Compton value for the cluster and the fluxes of the two main point sources in the field: SMM J140104+0252, and SMM J14009+0252 are found to be $y_{0}=(4.34\pm0.52\pm0.69)\times10^{-4}$, 6.5$\pm{2.0}\pm0.7$ mJy and 11.3$\pm{1.9}\pm1.1$ mJy, where the first error represents the statistical measurement error and the second error represents the estimated systematic error in the result. This measurement assumes the presence of dust emission from the cluster's central cD galaxy of $1.8\pm0.5$ mJy, based on higher frequency observations of Abell 1835. The cluster image represents one of the highest-significance SZ detections of a cluster in the positive region of the thermal SZ spectrum to date. The inferred central intensity is compared to other SZ measurements of Abell 1835 and this collection of results is used to obtain values for $y_{0} = (3.60\pm0.24)\times10^{-4}$ and the cluster peculiar velocity $v_{z} = -226\pm275$ km/s.Comment: 9 pages, 5 figure

Incidence of congenital abnormalities in Cape Town

No abstract availabl

Selective antagonism of A1 adenosinergic receptors strengthens the neuromodulation of sensorimotor network during epidural spinal stimulation

Although epidural spinal stimulation (ESS) results in promising therapeutic effects in individuals with spinal cord injury (SCI), its potential to generate functional motor recovery varies between individuals and remains largely unclear. However, both preclinical and clinical studies indicate the capacity of electrical and pharmacological interventions to synergistically increase engagement of spinal sensorimotor networks and regain motor function after SCI. This study explored whether selective pharmacological antagonism of the adenosine A1 receptor subtype synergizes with ESS, thereby increasing motor response. We hypothesized that selective pharmacological antagonism of A1 receptors during ESS would produce facilitatory effects in spinal sensorimotor networks detected as an increased amplitude of spinally-evoked motor potentials and sustained duration of ESS induced activity. Terminal experiments were performed in adult rats using trains of stereotyped pulses at 40 Hz delivered at L5 with local administration to the cord of 8-cyclopentyl-1,3-dipropylxanthine (DPCPX). We demonstrated that ESS combined with the blockage of A1 receptors increased the magnitude of the endogenous modulation and postponed the decay of responses that occur during ESS alone. Although DPCPX significantly increased the yield of repetitive stimulation in intact spinal cords, effects of A1 antagonism on motor evoked responses after an acute spinal transection were not detected. These studies support future investigation of the optimal dosage, methods of delivery, and systemic effects of the synergistic application of A1 antagonists and spinal stimulation in intact and injured spinal cord

Transplantable human motor networks as a neuron-directed strategy for spinal cord injury

To repair neural circuitry following spinal cord injury (SCI), neural stem cell (NSC) transplantation has held a primary focus; however, stochastic outcomes generate challenges driven in part by NSC differentiation and tumor formation. The recent ability to generate regionally specific neurons and their support cells now allows consideration of directed therapeutic approaches with pre-differentiated and networked spinal neural cells. Here, we form encapsulated, transplantable neuronal networks of regionally matched cervical spinal motor neurons, interneurons, and oligodendrocyte progenitor cells derived through trunk-biased neuromesodermal progenitors. We direct neurite formation in alginate-based neural ribbons to generate electrically active, synaptically connected networks, characterized by electrophysiology and calcium imaging before transplantation into rodent models of contused SCI for evaluation at 10-day and 6-week timepoints. The in vivo analyses demonstrate viability and retention of interconnected synaptic networks that readily integrate with the host parenchyma to advance goals of transplantable neural circuitry for SCI treatment

Neuregulin 1 confers neuroprotection in SOD1-linked amyotrophic lateral sclerosis mice via restoration of C-boutons of spinal motor neurons

Supplementary figures (Figure S1, S2, S3, and S4). (PDF 2135 kb

Albedo and Reflection Spectra of Extrasolar Giant Planets

We generate theoretical albedo and reflection spectra for a full range of extrasolar giant planet (EGP) models, from Jovian to 51-Pegasi class objects. Our albedo modeling utilizes the latest atomic and molecular cross sections, a Mie theory treatment of extinction by condensates, a variety of particle size distributions, and an extension of the Feautrier radiative transfer method which allows for a general treatment of the scattering phase function. We find that due to qualitative similarities in the compositions and spectra of objects within each of five broad effective temperature ranges, it is natural to establish five representative EGP albedo classes: a ``Jovian'' class (T$_{\rm eff} \lesssim 150$ K; Class I) with tropospheric ammonia clouds, a ``water cloud'' class (T$_{\rm eff} \sim 250$ K; Class II) primarily affected by condensed H$_2$O, a ``clear'' class (T$_{\rm eff} \gtrsim 350$ K; Class III) which lacks clouds, and two high-temperature classes: Class IV (900 K $\lesssim$ T$_{\rm{eff}}$ $\lesssim$ 1500 K) for which alkali metal absorption predominates, and Class V (T$_{\rm{eff}}$ $\gtrsim$ 1500 K and/or low surface gravity ($\lesssim$ 10$^3$ cm s$^{-2}$)) for which a high silicate layer shields a significant fraction of the incident radiation from alkali metal and molecular absorption. The resonance lines of sodium and potassium are expected to be salient features in the reflection spectra of Class III, IV, and V objects. We derive Bond albedos and effective temperatures for the full set of known EGPs and explore the possible effects of non-equilibrium condensed products of photolysis above or within principal cloud decks. As in Jupiter, such species can lower the UV/blue albedo substantially, even if present in relatively small mixing ratios.Comment: revised LaTeX manuscript accepted to Ap.J.; also available at http://jupiter.as.arizona.edu/~burrows/paper

TWIST1 promotes invasion through mesenchymal change in human glioblastoma

Background: Tumor cell invasion into adjacent normal brain is a mesenchymal feature of GBM and a major factor contributing to their dismal outcomes. Therefore, better understandings of mechanisms that promote mesenchymal change in GBM are of great clinical importance to address invasion. We previously showed that the bHLH transcription factor TWIST1 which orchestrates carcinoma metastasis through an epithelial mesenchymal transition (EMT) is upregulated in GBM and promotes invasion of the SF767 GBM cell line in vitro. Results: To further define TWIST1 functions in GBM we tested the impact of TWIST1 over-expression on invasion in vivo and its impact on gene expression. We found that TWIST1 significantly increased SNB19 and T98G cell line invasion in orthotopic xenotransplants and increased expression of genes in functional categories associated with adhesion, extracellular matrix proteins, cell motility and locomotion, cell migration and actin cytoskeleton organization. Consistent with this TWIST1 reduced cell aggregation, promoted actin cytoskeletal re-organization and enhanced migration and adhesion to fibronectin substrates. Individual genes upregulated by TWIST1 known to promote EMT and/or GBM invasion included SNAI2, MMP2, HGF, FAP and FN1. Distinct from carcinoma EMT, TWIST1 did not generate an E- to N-cadherin "switch" in GBM cell lines. The clinical relevance of putative TWIST target genes SNAI2 and fibroblast activation protein alpha (FAP) identified in vitro was confirmed by their highly correlated expression with TWIST1 in 39 human tumors. The potential therapeutic importance of inhibiting TWIST1 was also shown through a decrease in cell invasion in vitro and growth of GBM stem cells. Conclusions: Together these studies demonstrated that TWIST1 enhances GBM invasion in concert with mesenchymal change not involving the canonical cadherin switch of carcinoma EMT. Given the recent recognition that mesenchymal change in GBMs is associated with increased malignancy, these findings support the potential therapeutic importance of strategies to subvert TWIST1-mediated mesenchymal change

A Conditional Deletion of the NR1 Subunit of the NMDA Receptor in Adult Spinal Cord Dorsal Horn Reduces NMDA Currents and Injury-Induced Pain

To determine the importance of the NMDA receptor (NMDAR) in pain hypersensitivity after injury, the NMDAR1 (NR1) subunit was selectively deleted in the lumbar spinal cord of adult mice by the localized injection of an adenoassociated virus expressing Cre recombinase into floxed NR1 mice. NR1 subunit mRNA and dendritic protein are reduced by 80% in the area of the virus injection, and NMDA currents, but not AMPA currents, are reduced 86–88% in lamina II neurons. The spatial NR1 knock-out does not alter heat or cold paw-withdrawal latencies, mechanical threshold, or motor function. However, injury-induced pain produced by intraplantar formalin is reduced by 70%. Our results demonstrate conclusively that the postsynaptic NR1 receptor subunit in the lumbar dorsal horn of the spinal cord is required for central sensitization, the central facilitation of pain transmission produced by peripheral injury