Observations of the Ca II K line in Hel0830A dark points on August 3, 1985

Spectroheliograms taken in the light of He I 10830 A at the National Solar Observatory Vacuum Telescope on Kitt Peak were used to identify coronal holes and bright points (BPs). Target points were identified, coordinates calculated, and spectra recorded. For each spectrum, the difference in wavelength between the Ca II K minimum and the FeI reference line was calculated. It was noteworthy that the overall effect is a blueshift. It should be noted that if material of chromospheric density moves outward at this velocity, it could supply the mass flux of the solar wind if this chromospheric flow was concentrated in a few dozen sources, each of a diameter of a few arc seconds

Inhibition of biofilm growth on highly polycationic polyelectrolyte multilayers

Thesis (S.B.)--Massachusetts Institute of Technology, Dept. of Materials Science and Engineering, June 2008."May 16, 2008."Includes bibliographical references.The epithelial cell adhesion molecule E-cadherin is often down regulated during carcinoma progression and metastatic spread of tumors. However, the precise mechanism and molecular basis of metastasis promotion by E-cadherin loss is not completely understood. To investigate its role in metastasis, I utilized two distinct methods of E-cadherin inhibition that distinguish between E-cadherin's cell-cell adhesion and intracellular signaling functions. While the disruption of cell-cell contacts alone does not enable metastasis in vivo, the loss of E-cadherin protein does, through induction of an epithelial-to-mesenchymal transition (EMT), invasiveness and anoikis-resistance. E-cadherin binding partner f3-catenin is necessary but not sufficient for these phenotypes. In addition, gene expression analysis shows that E-cadherin loss results in the induction of multiple transcription factors, at least one of which, Twist, is necessary for E-cadherin loss-induced metastasis. These findings indicate that E-cadherin loss in tumors contributes to metastatic dissemination by inducing wide-ranging transcriptional and functional changes. In addition to promoting metastasis, loss of E-cadherin and the accompanying EMT renders cells resistant to conventional chemotherapeutic drugs. As the cells that have undergone an EMT represent the pool of cancer cells most competent to metastasize and lead to tumor recurrence, it is of vital importance to find therapies that effectively target such cells. Paired cell lines that differ in their differentiation state were utilized to discover compounds with selective toxicity against cells that have undergone an EMT. High-throughput screening of small molecule libraries resulted in a number of compounds that specifically affect the viability of cells that have undergone an EMT while having minimal cytotoxic effects on control epithelial cells. These studies establish a proof-of-principle for discovering compounds that target highly metastatic and otherwise chemotherapy resistant cancer cells.by Albert H. Park.S.B

Search for Boosted Dark Matter at ProtoDUNE

We propose the first experimental test of the inelastic boosted dark matter hypothesis, capitalizing on the new physics potential with the imminent data taking of the ProtoDUNE detectors. More specifically, we explore various experimental signatures at the cosmic frontier, arising in boosted dark matter scenarios, i.e., relativistic, inelastic scattering of boosted dark matter often created by the annihilation of its heavier component which usually comprises of the dominant relic abundance. Although features are unique enough to isolate signal events from potential backgrounds, vetoing a vast amount of cosmic background is rather challenging as the detectors are located on the ground. We argue, with a careful estimate, that such backgrounds nevertheless can be well under control by performing dedicated analyses after data acquisition. We then discuss some phenomenological studies which can be achieved with ProtoDUNE, employing a dark photon scenario as our benchmark dark-sector model.Comment: Supplemental material include

The ubiquitin receptor S5a/Rpn10 links centrosomal proteasomes with dendrite development in the mammalian brain

SummaryProteasomes drive the selective degradation of protein substrates with covalently linked ubiquitin chains in eukaryotes. Although proteasomes are distributed throughout the cell, specific biological functions of the proteasome in distinct subcellular locales remain largely unknown. We report that proteasomes localized at the centrosome regulate the degradation of local ubiquitin conjugates in mammalian neurons. We find that the proteasomal subunit S5a/Rpn10, a ubiquitin receptor that selects substrates for degradation, is essential for proteasomal activity at centrosomes in neurons and thereby promotes the elaboration of dendrite arbors in the rodent brain in vivo. We also find that the helix-loop-helix protein Id1 disrupts the interaction of S5a/Rpn10 with the proteasomal lid and thereby inhibits centrosomal proteasome activity and dendrite elaboration in neurons. Together, our findings define a function for a specific pool of proteasomes at the neuronal centrosome and identify a biological function for S5a/Rpn10 in the mammalian brain

Magnetization reversal by injection and transfer of spin: experiments and theory

Reversing the magnetization of a ferromagnet by spin transfer from a current, rather than by applying a magnetic field, is the central idea of an extensive current research. After a review of our experiments of current-induced magnetization reversal in Co/Cu/Co trilayered pillars, we present the model we have worked out for the calculation of the current-induced torque and the interpretation of the experiments

Natural killer cells attenuate cytomegalovirus-induced hearing loss in mice

<div><p>Congenital cytomegalovirus (CMV) infection is the most common non-hereditary cause of sensorineural hearing loss (SNHL) yet the mechanisms of hearing loss remain obscure. Natural Killer (NK) cells play a critical role in regulating murine CMV infection via NK cell recognition of the Ly49H cell surface receptor of the viral-encoded m157 ligand expressed at the infected cell surface. This Ly49H NK receptor/m157 ligand interaction has been found to mediate host resistance to CMV in the spleen, and lung, but is much less effective in the liver, so it is not known if this interaction is important in the context of SNHL. Using a murine model for CMV-induced labyrinthitis, we have demonstrated that the Ly49H/m157 interaction mediates host resistance in the temporal bone. BALB/c mice, which lack functional Ly49H, inoculated with mCMV at post-natal day 3 developed profound hearing loss and significant outer hair cell loss by 28 days of life. In contrast, C57BL/6 mice, competent for the Ly49H/m157 interaction, had minimal hearing loss and attenuated outer hair cell loss with the same mCMV dose. Administration of Ly49H blocking antibody or inoculation with a mCMV viral strain deleted for the m157 gene rendered the previously resistant C57BL/6 mouse strain susceptible to hearing loss to a similar extent as the BALB/c mouse strain indicating a direct role of the Ly49H/m157 interaction in mCMV-dependent hearing loss. Additionally, NK cell recruitment to sites of infection was evident in the temporal bone of inoculated susceptible mouse strains. These results demonstrate participation of NK cells in protection from CMV-induced labyrinthitis and SNHL in mice.</p></div

Quantification of Ultrasound Correlation‐Based Flow Velocity Mapping and Edge Velocity Gradient Measurement

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/135662/1/jum201332101815.pd

Interface Depinning in the Absence of External Driving Force

We study the pinning-depinning phase transition of interfaces in the quenched Kardar-Parisi-Zhang model as the external driving force $F$ goes towards zero. For a fixed value of the driving force we induce depinning by increasing the nonlinear term coefficient $\lambda$, which is related to lateral growth, up to a critical threshold. We focus on the case in which there is no external force applied (F=0) and find that, contrary to a simple scaling prediction, there is a finite value of $\lambda$ that makes the interface to become depinned. The critical exponents at the transition are consistent with directed percolation depinning. Our results are relevant for paper wetting experiments, in which an interface gets moving with no external driving force.Comment: 4 pages, 3 figures included, uses epsf. Submitted to PR

Why social networks are different from other types of networks

We argue that social networks differ from most other types of networks, including technological and biological networks, in two important ways. First, they have non-trivial clustering or network transitivity, and second, they show positive correlations, also called assortative mixing, between the degrees of adjacent vertices. Social networks are often divided into groups or communities, and it has recently been suggested that this division could account for the observed clustering. We demonstrate that group structure in networks can also account for degree correlations. We show using a simple model that we should expect assortative mixing in such networks whenever there is variation in the sizes of the groups and that the predicted level of assortative mixing compares well with that observed in real-world networks.Comment: 9 pages, 2 figure

Geographic constraints on social network groups

Social groups are fundamental building blocks of human societies. While our social interactions have always been constrained by geography, it has been impossible, due to practical difficulties, to evaluate the nature of this restriction on social group structure. We construct a social network of individuals whose most frequent geographical locations are also known. We also classify the individuals into groups according to a community detection algorithm. We study the variation of geographical span for social groups of varying sizes, and explore the relationship between topological positions and geographic positions of their members. We find that small social groups are geographically very tight, but become much more clumped when the group size exceeds about 30 members. Also, we find no correlation between the topological positions and geographic positions of individuals within network communities. These results suggest that spreading processes face distinct structural and spatial constraints.Comment: 10 pages, 5 figure