Love Sends A Little Gift of Roses

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Love Sends a Little Gift of Roses

[VERSE 1]Take thou my gift,My offering of roses,Cull\u27d from my garden,Sweet with twilight dew;If just one flow\u27r upon your breast reposesLife shall forever hold no rose but you. [REFRAIN]Love sends a little gift of roses,Breathing a pray\u27r unto my posies,Torn from my heart as twilight closes,Asking this, only thisOne heart to grow a little tender,Two eyes to glow with love\u27s own splendour,Two lips to give in sweet surrenderJust a kiss, just a kiss. [VERSE 2]Take thou my gift,And be it joy or sorrow,Think ere my roses fadeAnd fall apart;With each sweet bloomThat you may scorn tomorrow,I send to you for joy or pain my heart. [REFRAIN

June Brought the Roses

[Verse 1]Red leaves, faded and dead leaves, Seabirds flown; ‘Round me winter had found me Sad and lone, Life seemed one long December, Skies were grey,Dearest, then I remember,One sweet day. [Verse 2] Sad hours all will be glad hours,Come what may, New skies wonderfil blue skies, Light my way, Winter shadows returning,Hold no fearsWith Love’s light everburning, Through the years. [Refrain]June brought the roses so fragrant with dew, June brought the sunbeams, and when they peeoped through,Songbirds were singing Melodies ringing, Bidding the world love anew; There in Love’s garden my dreams all came true,I found a red rose, the fairest that grew,After the grey days, After the May days. June brought the roses and you

Studies of the Gaviota Slide Offshore Southern California

We are engaged in a study of a seafloor landslide off the coast of Santa Barbara, California. A large scar there remains from the Goleta slide, a well studied feature (1.51 km3 of failed material) that likely failed several thousand years ago. A smaller neighboring feature, the Gaviota slide (0.02 km3 of failed material), was probably triggered during the 1812 Santa Barbara earthquake. Our investigations started in 2004 with a chirp sonar survey. The survey revealed a relationship between a “crack” in the sediment propagating from the Gaviota slide’s headwall and a thrust fault clearly seen in the subsurface layers. In the next phase of our project we are applying three new time-lapse seafloor geodetic techniques that vary in spatial and temporal resolution. One method uses optical fibers stretched and buried in the sediment to monitor creep. Each cable has an optical system that measures the absolute length of the stretched optical fiber with a precision of 1 mm every hour. The cables vary in length from 250 m to 750 m. A second system consists of an array of precise acoustic transponders on the seafloor interrogated by several buoyantly suspended command nodes. Offshore engineering tests of these reveal a precision of 5 mm over baselines up to 2 km. Finally, we are developing an AUV-borne precision mapping capability that promises to provide a monitor of seafloor shape changes that occur over tracklines of many kilometers in length with a precision goal of 10 cm. We are currently preparing these geodetic monitoring tools for deployment across a presumed future headwall near the Gaviota slide in a nested fashion to provide redundancy and a means to compare resolutions

Spatial Aggregation Methods for Investigating the MAUP Effects in Migration Analysis

In this paper, we investigate the effects of scale and zone configuration on migration indicators and spatial interaction model parameters using a software system known as the IMAGE Studio. Internal migration flows in the United Kingdom and the local authority districts between which they move are aggregated into sets of increasingly fewer and larger polygons using alternative zone design algorithms. Indicators of migration intensity, impact and distance are revealed to vary significantly by scale but less so by zonation, whereas migration effectiveness and distance show greater scale independence but more sensitivity to zone configuration. Equal area and population optimised regions improve the quality of measures to a certain degree depending upon the imposition of shape constraints

The Chemokine MIP1α/CCL3 Determines Pathology in Primary RSV Infection by Regulating the Balance of T Cell Populations in the Murine Lung

BACKGROUND: CD8 T cells assist in the clearance of respiratory syncytial virus (RSV) infection from the lungs. However, disease after RSV infection is in part caused by excessive T cell activity, and a balance is therefore needed between beneficial and harmful cellular immune responses. The chemokine CCL3 (MIP1alpha) is produced following RSV infection and is broadly chemotactic for both T cells and natural killer (NK) cells. We therefore investigated its role in RSV disease. METHODOLOGY/PRINCIPAL FINDINGS: CCL3 was produced biphasically, in both the early (day 1) and late (day 6-7) stages of infection. CCL3 depletion did not alter the recruitment of natural killer (NK) cells to the lungs during the early stage, but depletion did affect the later adaptive phase. While fewer T cells were recruited to the lungs of either CCL3 knockout or anti-CCL3 treated RSV infected mice, more RSV-specific pro-inflammatory T cells were recruited to the lung when CCL3 responses were impaired. This increase in RSV-specific pro-inflammatory T cells was accompanied by increased weight loss and illness after RSV infection. CONCLUSIONS/SIGNIFICANCE: CCL3 regulates the balance of T cell populations in the lung and can alter the outcome of RSV infection. Understanding the role of inflammatory mediators in the recruitment of pathogenic T cells to the lungs may lead to novel methods to control RSV disease

Exercise attenuates neuropathology and has greater benefit on cognitive than motor deficits in the R6/1 Huntington's disease mouse model

Huntington's disease (HD) is a neurodegenerative disease caused by a mutation within the huntingtin gene that induces degeneration within the striatal nuclei, progressing to widespread brain atrophy and death. The neurodegeneration produces symptoms that reflect a corticostriatal disconnection syndrome involving motor, cognitive and psychiatric disturbances. Environmental enrichment has been demonstrated to be beneficial to patients with neurological disorders, with exercise being central to this effect. Rodent studies have confirmed exercise-induced neurogenesis and increased growth factor levels in the brain and improved behavioural function. The present study sought to determine whether an extended regime of exercise could retard disease progression in the R6/1 mouse model of HD. The study was designed specifically with a translational focus, selecting behavioural assessments with high clinical predictive validity. We found that exercise improved gait function in both control and HD mice and selectively improved performance in the R6/1 mice on a motor coordination aspect of the balance beam task. Exercise also retarded the progression of cognitive dysfunction on water T-maze procedural and reversal learning probes presented serially to probe cognitive flexibility. In addition, exercise reduced striatal neuron loss in the R6/1 mice but increased striatal neuronal intra-nuclear inclusion size and number relative to non-exercised R6/1 mice which demonstrated increased numbers of extra-neuronal inclusions, suggesting that the functional effects were striatally mediated. These results confirm and extend those from previous studies that demonstrate that HD may be amenable to exercise-mediated therapeutics, but suggest that the impact of such interventions may be primarily cognitive

Selective Expression of a Stable Cell Surface Molecule on Type 2 but Not Type 1 Helper T Cells

T helper cell type 1 (Th1) and 2 (Th2) are central to immune regulation. However, no stable cell surface marker capable of distinguishing and separating these two subsets of CD4+ cells has yet been found. Using differential display PCR, we have identified a gene encoding a cell membrane bound molecule, originally designated ST2L, T1, DER4, or Fit, expressed constitutively and stably on the surface of murine Th2s, but not Th1s even after stimulation with a range of immunological stimuli. Antibody against a peptide derived from ST2L strongly and stably labeled the surface of cloned Th2s but not Th1s, and Th2s but not Th1s derived from naive T cells of ovalbumin T cell receptor–α/β transgenic mice. Three-color single cell flow cytometric analysis shows that cell surface ST2L coexpressed with intracellular interleukin (IL)-4, but not with interferon (IFN)-γ. The antibody selectively lysed Th2s in vitro in a complement-dependent manner. In vivo, it enhanced Th1 responses by increasing IFN-γ production and decreasing IL-4 and IL-5 synthesis. It induced resistance to Leishmania major infection in BALB/c mice and exacerbated collagen-induced arthritis in DBA/1 mice. Thus, ST2L is a stable marker distinguishing Th2s from Th1s and is also associated with Th2 functions. Hence, it may be a target for therapeutic intervention

CXCL10/CXCR3-mediated responses promote immunity to respiratory syncytial virus infection by augmenting dendritic cell and CD8 + T cell efficacy

The induction of inflammatory cytokines during respiratory viral infections contributes to both disease pathogenesis and resolution. The present studies investigated the role of the chemokine CXCL10 and its specific receptor, CXCR3, in the host response to pulmonary respiratory syncytial virus (RSV) infection. Antibody-mediated neutralization of CXCL10 resulted in a significant increase in disease pathogenesis, including airway hyperresponsiveness (AHR), mucus gene expression, and impaired viral clearance. When the pulmonary cytokine levels were examined, only type I IFN and IL-12p70 were significantly reduced. These latter observations were reflected in reduced dendritic cell (DC) numbers and DC maturation in the lungs of RSV-infected mice treated with anti-CXCL10. Neutralization of the only known receptor for CXCL10, CXCR3, resulted in similar increases in pathogenic responses. When bone marrow-derived DC were incubated with CXCL10 and RSV, an up-regulation of type I IFN was observed. In addition, T lymphocytes were also examined and a significant decrease in the number of RSV M2 peptide-specific CD8 + T cells was identified. These findings highlight a previously unappreciated role for the CXCL10:CXCR3 signaling axis in RSV-infected animals by recruiting virus-specific T cells into the lung and promoting viral clearance.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/60446/1/2168_ftp.pd