Life histories determine divergent population trends for fishes under climate warming

Most marine fish species express life-history changes across temperature gradients, such as faster growth, earlier maturation, and higher mortality at higher temperature. However, such climate-driven effects on life histories and population dynamics remain unassessed for most fishes. For 332 Indo-Pacific fishes, we show positive effects of temperature on body growth (but with decreasing asymptotic length), reproductive rates (including earlier age-at-maturation), and natural mortality for all species, with the effect strength varying among habitat-related species groups. Reef and demersal fishes are more sensitive to temperature changes than pelagic and bathydemersal fishes. Using a life table, we show that the combined changes of life histories upon increasing temperature tend to facilitate population growth for slow life-history populations, but reduce it for fast life-history ones. Within our data, lower proportions (25-30%) of slow life-history fishes but greater proportions of fast life-history fishes (42-60%) show declined population growth rates under 1 °C warming. Together, these findings suggest prioritizing sustainable management for fast life-history species

CDK Inhibitor p18INK4c Is Required for the Generation of Functional Plasma Cells

AbstractB cell terminal differentiation is associated with the onset of high-level antibody secretion and cell cycle arrest. Here the cyclin-dependent kinase (CDK) inhibitor p18INK4c is shown to be required within B cells for both terminating cell proliferation and differentiation of functional plasma cells. In its absence, B cells hyperproliferate in germinal centers and extrafollicular foci in response to T-dependent antigens but serum antibody titers are severely reduced, despite unimpaired germinal center formation, class switch recombination, variable region-directed hypermutation, and differentiation to antibody-containing plasmacytoid cells. The novel link between cell cycle control and plasma cell differentiation may, at least in part, relate to p18INK4c inhibition of CDK6. Cell cycle arrest mediated by p18INK4C is therefore requisite for the generation of functional plasma cells

Surface and Temporal Biosignatures

Recent discoveries of potentially habitable exoplanets have ignited the prospect of spectroscopic investigations of exoplanet surfaces and atmospheres for signs of life. This chapter provides an overview of potential surface and temporal exoplanet biosignatures, reviewing Earth analogues and proposed applications based on observations and models. The vegetation red-edge (VRE) remains the most well-studied surface biosignature. Extensions of the VRE, spectral "edges" produced in part by photosynthetic or nonphotosynthetic pigments, may likewise present potential evidence of life. Polarization signatures have the capacity to discriminate between biotic and abiotic "edge" features in the face of false positives from band-gap generating material. Temporal biosignatures -- modulations in measurable quantities such as gas abundances (e.g., CO2), surface features, or emission of light (e.g., fluorescence, bioluminescence) that can be directly linked to the actions of a biosphere -- are in general less well studied than surface or gaseous biosignatures. However, remote observations of Earth's biosphere nonetheless provide proofs of concept for these techniques and are reviewed here. Surface and temporal biosignatures provide complementary information to gaseous biosignatures, and while likely more challenging to observe, would contribute information inaccessible from study of the time-averaged atmospheric composition alone.Comment: 26 pages, 9 figures, review to appear in Handbook of Exoplanets. Fixed figure conversion error

Search for flavor-changing neutral currents and lepton-family-number violation in two-body D0 decays

Results of a search for the three neutral charm decays, D0 -> mu e, D0 -> mu mu, and D0 -> e e, are presented. This study was based on data collected in Experiment 789 at the Fermi National Accelerator Laboratory using 800 GeV/c proton-Au and proton-Be interactions. No evidence is found for any of the decays. Upper limits on the branching ratios, at the 90% confidence level, are obtained.Comment: 28 pages, 18 figures. Submitted to Physical Review

Exoplanet Characterization and the Search for Life

Over 300 extrasolar planets (exoplanets) have been detected orbiting nearby stars. We now hope to conduct a census of all planets around nearby stars and to characterize their atmospheres and surfaces with spectroscopy. Rocky planets within their star's habitable zones have the highest priority, as these have the potential to harbor life. Our science goal is to find and characterize all nearby exoplanets; this requires that we measure the mass, orbit, and spectroscopic signature of each one at visible and infrared wavelengths. The techniques for doing this are at hand today. Within the decade we could answer long-standing questions about the evolution and nature of other planetary systems, and we could search for clues as to whether life exists elsewhere in our galactic neighborhood.Comment: 7 pages, 2 figures, submitted to Astro2010 Decadal Revie

Coordinated Silencing of MYC-Mediated miR-29 by HDAC3 and EZH2 as a Therapeutic Target of Histone Modification in Aggressive B-Cell Lymphomas

We investigated the transcriptional and epigenetic repression of miR-29 by MYC, HDAC3, and EZH2 in mantle cell lymphoma and other MYC-associated lymphomas. We demonstrate that miR-29 is repressed by MYC through a corepressor complex with HDAC3 and EZH2. MYC contributes to EZH2 upregulation via repression of the EZH2 targeting miR-26a, and EZH2 induces MYC via inhibition of the MYC targeting miR-494 to create positive feedback. Combined inhibition of HDAC3 and EZH2 cooperatively disrupted the MYC-EZH2-miR-29 axis, resulting in restoration of miR-29 expression, downregulation of miR-29-targeted genes, and lymphoma growth suppression in vitro and in vivo. These findings define a MYC-mediated miRNA repression mechanism, shed light on MYC lymphomagenesis mechanisms, and reveal promising therapeutic targets for aggressive B-cell malignancies

Retrospective analysis of 119 Chinese noninflammatory locally advanced breast cancer cases treated with intravenous combination of vinorelbine and epirubicin as a neoadjuvant chemotherapy: a median follow-up of 63.4 months

<p>Abstract</p> <p>Background</p> <p>This study is a retrospective evaluation of the efficacy of neoadjuvant chemotherapy (NC) with a vinorelbine (V) and epirubicin (E) intravenous combination regimen and is aimed at identification of predictive markers for the long-term outcome in noninflammatory locally advanced breast cancer (NLABC).</p> <p>Methods</p> <p>One-hundred-and-nineteen patients with NLABC were identified from September 2001 to May 2006. Analysis was performed in March 2008, with a median follow-up of 63.4 months (range, 9-76 months). All patients were diagnosed with invasive breast cancer using 14 G core needle biopsy and treated with three cycles of VE before surgery. Local-regional radiotherapy was offered to all patients after the completion of chemotherapy followed by hormonal therapy according to hormone receptor status. Tissue sections cut from formalin-fixed paraffin-embedded blocks from biopsy specimens and postoperative tumor tissues were stained for the presence of estrogen receptor (ER), progesterone receptor (PgR), HER-2 (human epidermal growth factor receptor-2), and MIB-1(Ki-67).</p> <p>Results</p> <p>Patients characteristics were median age 52 years (range: 25-70 years); clinical TNM stage, stage IIB (n = 32), stage IIIA (n = 56), stage IIIB (n = 22) and stage IIIC (n = 9). All patients were evaluable for response: clinically complete response was documented in 27 patients (22.7%); 78 (65.6%) obtained partial response; stable disease was observed in 13 (10.9%); 1 patient (0.8%) had progressive disease. Pathological complete response was found in 22 cases (18.5%). Seventy-five patients were alive with no recurrence after a median follow-up of 63.4 months, the 5-year rates for disease-free survival and overall survival were 58.7% and 71.3%, respectively, after the start of NC. On multivariate analysis, the independent variables associated with increased risk of relapse and death were high pre-Ki-67(p = 0.012, p = 0.017, respectively), high post-Ki-67 expression (p = 0.045, p = 0.001, respectively), and non-pCR (p = 0.034, p = 0.027, respectively). A significantly increased risk of death was associated with lack of pre-ER expression (p = 0.002). Among patients with non-pCR, those with a pathological response at the tumor site with special involvement (i.e. skin, vessel and more than one quadrant) were at a higher risk of disease relapse and death (p < 0.001, p = 0.001, respectively).</p> <p>Conclusion</p> <p>This study suggests the promising use of a VE regimen as NC for Chinese NLABC after a median follow-up of 63.4 months. Pathological response in the tumor site, pre-Ki-67 and post-Ki-67 expression, and pre-ER expression were the important variables that predicted long-term outcome. Patients with pathological special involvement at the primary site after NC had the lowest survival rates.</p

Forming-free resistive switching of tunable ZnO films grown by atomic layer deposition

Undoped ZnO thin films with tunable electrical properties have been achieved by adjusting the O2 plasma time in the plasma enhanced atomic layer deposition process. The structural, compositional and electrical properties of the deposited ZnO films were investigated by various characterization techniques. By tuning the plasma exposure from 2 to 8 s, both resistivities and carrier concentrations of the resultant ZnO films can be modulated by up to 3 orders of magnitude. Forming-free TiN/ZnO/TiN resistive memory devices have been achieved by choosing the ZnO film with the plasma exposure time of 6 s. This deposition method offers a great potential for producing other un-doped metal oxides with tunable properties as well as complex multilayer structures in a single deposition

Down-regulation of GRP78 is associated with the sensitivity of chemotherapy to VP-16 in small cell lung cancer NCI-H446 cells

<p>Abstract</p> <p>Background</p> <p>Chemotherapy resistance remains a major obstacle for the treatment of small cell lung cancer (SCLC). Glucose-regulated protein 78 (GRP78), an endoplasmic reticulum chaperone, plays a critical role in chemotherapy resistance in some cancers. However, whether the suppression of the chaperone can enhance the sensitivity of chemotherapy in SCLC is still unclear.</p> <p>Methods</p> <p>The SCLC NCI-H446 cells were divided into three groups: BAPTA-AM→A23187-treated group, A23187-treated group and control-group. Immunofluorescence, western blot and RT-PCR were used to assess the expression of GRP78 at both protein and mRNA levels. Cell apoptosis and the cell cycle distributions of the cells were analyzed by flow cytometry in order to evaluate the therapeutic sensitivity to VP-16.</p> <p>Results</p> <p>The expression of GRP78 at both protein and mRNA levels in the BAPTA-AM→A23187-treated cells dramatically decreased as compared to that in both A23187-treated and control groups. After treatment by VP-16, the percentage of apoptotic cells in BAPTA-AM→A23187-treated cells were: 33.4 ± 1.01%, 48.2 ± 1.77%, 53.0 ± 1.43%, 56.5 ± 2.13%, respectively, corresponding to the concentrations of BAPTA-AM 10, 15, 25, 40 μM, which was statistically significant high in comparison with the A23187-treated group and untreated-group (7.18 ± 1.03% and 27.8 ± 1.45%, respectively, p < 0.05). The results from analysis of cell cycle distribution showed that there was a significantly decreased in G₁phase and a dramatically increased in S phase for the BAPTA-AM→A23187-treated cells as compared with the untreated cells.</p> <p>Conclusion</p> <p>BAPTA-AM is a strong inhibitor of GRP78 in the NCI-H446 cell line, the down-regulation of GRP78 can significantly increase the sensitivity to VP-16. The suppression of GRP78 may offer a new surrogated therapeutic approach to the clinical management of lung cancer.</p