Analysis on the hull girder ultimate strength of a bulk carrier using simplified method based on an incremental-iterative approach

The hull girder ultimate strength of a typical bulk carrier is analyzed using a simplified method based on an incremental-iterative approach. First, vertical bending moment is examined by seven different methods. The moment versus curvature curves and the values of the ultimate longitudinal moments at collapse states are determined for both hogging and sagging cases. Second, the ultimate strength under coupled vertical and horizontal bending moment is accounted. An interaction curve is obtained, which corresponds to the results of series of calculation for the ship hull subject to bending conditions with different angles of curvature. It is found that the interaction curve is asymmetrical because the hull cross section is not symmetrical with respect to the horizontal axis and the structural response of the elements under compression is different from that under tension due to nonlinearity caused by buckling. The angles of the resultant bending moment vector and that of the curvature vector are different in investigated cases. The interaction design equations proposed by other researches are also addressed to discuss the results presented by this study

Spatial selectivity in human ventrolateral prefrontal cortex

The functional organization of lateral prefrontal cortex is not well understood, and there is debate as to whether the dorsal and ventral aspects mediate distinct spatial and non-spatial functions, respectively. We show for the first time that recordings from human ventrolateral prefrontal cortex show spatial selectivity, supporting the idea that ventrolateral prefrontal cortex is involved in spatial processing. Our results also indicate that prefrontal cortex may be a source of control signals for neuroprosthetic applications

Ataxia with oculomotor apraxia type 2: a clinical, pathologic, and genetic study

BACKGROUND: Ataxia with oculomotor apraxia type 2 (AOA2) is characterized by onset between age 10 and 22 years, cerebellar atrophy, peripheral neuropathy, oculomotor apraxia (OMA), and elevated serum alpha-fetoprotein (AFP) levels. Recessive mutations in SETX have been described in AOA2 patients. OBJECTIVE: To describe the clinical features of AOA2 and to identify the SETX mutations in 10 patients from four Italian families. METHODS: The patients underwent clinical examination, routine laboratory tests, nerve conduction studies, sural nerve biopsy, and brain MRI. All were screened for SETX mutations. RESULTS: All the patients had cerebellar features, including limb and truncal ataxia, and slurred speech. OMA was observed in two patients, extrapyramidal symptoms in two, and mental impairment in three. High serum AFP levels, motor and sensory axonal neuropathy, and marked cerebellar atrophy on MRI were detected in all the patients who underwent these examinations. Sural nerve biopsy revealed a severe depletion of large myelinated fibers in one patient, and both large and small myelinated fibers in another. Postmortem findings are also reported in one of the patients. Four different homozygous SETX mutations were found (a large-scale deletion, a missense change, a single-base deletion, and a splice-site mutation). CONCLUSIONS: The clinical phenotype of oculomotor apraxia type 2 is fairly homogeneous, showing only subtle intrafamilial variability. OMA is an inconstant finding. The identification of new mutations expands the array of SETX variants, and the finding of a missense change outside the helicase domain suggests the existence of at least one more functional region in the N-terminus of senataxin

Remanence effects in the electrical resistivity of spin glasses

We have measured the low temperature electrical resistivity of Ag : Mn mesoscopic spin glasses prepared by ion implantation with a concentration of 700 ppm. As expected, we observe a clear maximum in the resistivity (T ) at a temperature in good agreement with theoretical predictions. Moreover, we observe remanence effects at very weak magnetic fields for the resistivity below the freezing temperature Tsg: upon Field Cooling (fc), we observe clear deviations of (T ) as compared with the Zero Field Cooling (zfc); such deviations appear even for very small magnetic fields, typically in the Gauss range. This onset of remanence for very weak magnetic fields is reminiscent of the typical signature on magnetic susceptibility measurements of the spin glass transition for this generic glassy system

Concomitant Tumor Immunity to a Poorly Immunogenic Melanoma Is Prevented by Regulatory T Cells

Concomitant tumor immunity describes immune responses in a host with a progressive tumor that rejects the same tumor at a remote site. In this work, concomitant tumor immunity was investigated in mice bearing poorly immunogenic B16 melanoma. Progression of B16 tumors did not spontaneously elicit concomitant immunity. However, depletion of CD4+ T cells in tumor-bearing mice resulted in CD8+ T cell–mediated rejection of challenge tumors given on day 6. Concomitant immunity was also elicited by treatment with cyclophosphamide or DTA-1 monoclonal antibody against the glucocorticoid-induced tumor necrosis factor receptor. Immunity elicited by B16 melanoma cross-reacted with a distinct syngeneic melanoma, but not with nonmelanoma tumors. Furthermore, CD8+ T cells from mice with concomitant immunity specifically responded to major histocompatibility complex class I–restricted epitopes of two melanocyte differentiation antigens. RAG1−/− mice adoptively transferred with CD8+ and CD4+ T cells lacking the CD4+CD25+ compartment mounted robust concomitant immunity, which was suppressed by readdition of CD4+CD25+ cells. Naturally occurring CD4+CD25+ T cells efficiently suppressed concomitant immunity mediated by previously activated CD8+ T cells, demonstrating that precursor regulatory T cells in naive hosts give rise to effective suppressors. These results show that regulatory T cells are the major regulators of concomitant tumor immunity against this weakly immunogenic tumor

Intermediate Mass Black Hole Formation in compact Young Massive Star Clusters

Young dense massive star clusters are a promising environment for the formation of intermediate mass black holes (IMBHs) through collisions. We present a set of 80 simulations carried out with Nbody6++GPU of 10 initial conditions for compact $\sim 7 \times 10^4 M_{\odot}$ star clusters with half-mass radii $R_\mathrm{h} \lesssim 1 pc$, central densities $\rho_\mathrm{core} \gtrsim 10^5 M_\odot pc^{-3}$, and resolved stellar populations with 10\% primordial binaries. Very massive stars (VMSs) with masses up to $\sim 400 M_\odot$ grow rapidly by binary exchange and three-body scattering events with main sequences stars in hard binaries. Assuming that in VMS - stellar BH collisions all stellar material is accreted onto the BH, IMBHs with masses up to $M_\mathrm{BH} \sim 350 M_\odot$ can form on timescales of $\lesssim 15$ Myr. This process was qualitatively predicted from Monte Carlo MOCCA simulations. Despite the stochastic nature of the process - typically not more than 3/8 cluster realisations show IMBH formation - we find indications for higher formation efficiencies in more compact clusters. Assuming a lower accretion fraction of 0.5 for VMS - BH collisions, IMBHs can also form. The process might not work for accretion fractions as low as 0.1. After formation, the IMBHs can experience occasional mergers with stellar mass BHs in intermediate mass-ratio inspiral events (IMRIs) on a 100 Myr timescale. Realised with more than $10^5$ stars, 10 \% binaries, the assumed stellar evolution model with all relevant evolution processes included and 300 Myr simulation time, our large suite of simulations indicates that IMBHs of several hundred solar masses might form rapidly in massive star clusters right after their birth while they are still compact.Comment: Submitte

The endogenous caspase-8 inhibitor c-FLIPL regulates ER morphology and crosstalk with mitochondria

Components of the death receptors-mediated pathways like caspase-8 have been identified in complexes at intracellular membranes to spatially restrict the processing of local targets. In this study, we report that the long isoform of the cellular FLICE-inhibitory protein (c-FLIPL), a well- known inhibitor of the extrinsic cell death initiator caspase-8, localizes at the endoplasmic reticulum (ER) and mitochondria-associated membranes (MAMs). ER morphology was disrupted and ER Ca2+-release as well as ER-mitochondria tethering were decreased in c-FLIP-/- mouse embryonic fibroblasts (MEFs). Mechanistically, c-FLIP ablation resulted in enhanced basal caspase-8 activation and in caspase-mediated processing of the ER-shaping protein reticulon-4 (RTN4) that was corrected by re-introduction of c-FLIPL and caspase inhibition, resulting in the recovery of a normal ER morphology and ER-mitochondria juxtaposition. Thus, the caspase-8 inhibitor c-FLIPL emerges as a component of the MAMs signaling platforms, where caspases appear to regulate ER morphology and ER-mitochondria crosstalk by impinging on ER-shaping proteins like the RTN4

The mass-radius relation of young stars from K2

Evolutionary models of pre-main sequence stars remain largely uncalibrated, especially for masses below that of the Sun, and dynamical masses and radii pose valuable tests of these theoretical models. Stellar mass dependent features of star formation (such as disk evolution, planet formation, and even the IMF) are fundamentally tied to these models, which implies a systematic uncertainty that can only be improved with precise measurements of calibrator stars. We will describe the discovery and characterization of ten eclipsing binary systems in the Upper Scorpius star-forming region from K2 Campaign 2 data, spanning from B stars to the substellar boundary. We have obtained complementary RV curves, spectral classifications, and high-resolution imaging for these targets; the combination of these data yield high-precision masses and radii for the binary components, and hence a dense sampling of the (nominally coeval) mass-radius relation of 10 Myr old stars. We already reported initial results from this program for the young M4.5 eclipsing binary UScoCTIO 5 (Kraus et al. 2015), demonstrating that theoretically predicted masses are discrepant by ~50% for low-mass stars. K2's unique radius measurements allow us to isolate the source of the discrepancy: models of young stars do not predict luminosities that are too low, as is commonly thought, but rather temperatures that are too warm.http://adsabs.harvard.edu/abs/2016AAS...22723612KPublished versio