The Stratiform Radiation Effect on Tropical Organized Deep Convection

Idealized studies of self-aggregation have implicated the importance of longwave (LW) cloud-radiative forcing (CRF) in facilitating the upscale development of moist convection. While different cloud structures are known to have distinct CRF, the relative role of distinct cloud and precipitation types in driving upscale development through radiative feedback is largely unexplored. Considering the impact CRF has on convection, we hypothesize that different cloud modes have different effects on mesoscale tropical convection through radiative feedback. We test this hypothesis by analyzing output from Weather Research and Forecasting (WRF) model simulations of Super Typhoon Haiyan. Using a novel column-by-column precipitation classification scheme, we use this model output to identify the relative contribution of 5 cloud types to the direct LW radiative forcing and the upscale development of convection via LW moist static energy variance. Results indicate that stratiform and anvil regions contribute dominantly to the domain averages of these variables. We next compared the control simulation (CTL) to sensitivity tests that exclude cloud-radiative feedback (NCRF) either everywhere or only in specific cloud types. These tests indicate that the upscale development of deep convection that manifests in tropical cyclone (TC) genesis is accelerated by CRF, especially of that in stratiform regions. There is a growing consensus from observations that the areal growth of stratiform precipitation is a key precursor to TC genesis and intensification. This observational finding presents a conundrum, given that stratiform precipitation is directly tied to downdrafts, and hence ventilation. Therefore, we hypothesize that the cloud-radiative effect within stratiform cloud regions weakens downdrafts, allowing the environment to moisten more easily. Analysis shows that CTL tests have less downward vertical mass flux in the mid to lower troposphere, indicating weaker (and/or fewer) downdrafts, than that of the NCRF tests, with the greatest differences being in stratiform regions. These findings support our hypothesis that cloud-radiative effects in the stratiform regions weaken downdrafts in developing TCs, in turn allowing the environment to moisten more easily. Understanding the importance of cloud type CRF, especially that of stratiform, could provide insight on the development of tropical convection and TC genesis

A 1-10 GHz distributed amplifier

This graduate project makes use of the principles of distributed amplification in the design and fabrication of a microwave amplifier which operates over a decade of bandwidth. The relationship between a lumped transmission line and a distributed amplifier is explained, showing why the distributed amplifier is an inherently broadband structure. Simplified models are constructed and analyzed, illustrating these fundamental relationships and giving empirical formulas for expected performance. Measured transistor data are then used in the design of a distributed amplifier. This amplifier was fabricated and measured, and compared to the computer analysis. The final design led to an amplifier which gave good agreement with predicted performance.California State University, Northridge. Department of Engineering.Includes bibliographical references (pages 22-23

Signatures of Many-Body Localization in a Controlled Open Quantum System

In the presence of disorder, an interacting closed quantum system can undergo many-body localization (MBL) and fail to thermalize. However, over long times, even weak couplings to any thermal environment will necessarily thermalize the system and erase all signatures of MBL. This presents a challenge for experimental investigations of MBL since no realistic system can ever be fully closed. In this work, we experimentally explore the thermalization dynamics of a localized system in the presence of controlled dissipation. Specifically, we find that photon scattering results in a stretched exponential decay of an initial density pattern with a rate that depends linearly on the scattering rate. We find that the resulting susceptibility increases significantly close to the phase transition point. In this regime, which is inaccessible to current numerical studies, we also find a strong dependence on interactions. Our work provides a basis for systematic studies of MBL in open systems and opens a route towards extrapolation of closed-system properties from experimentsWe acknowledge financial support by the European Commission (UQUAM, AQuS) and the Nanosystems Initiative Munich (NIM). Work at Strathclyde is supported by the EOARD via AFOSR Grant No. FA2386-14-1-5003. This research was supported in part by the National Science Foundation under Grant No. NSF PHY11-25915. M. H. F. acknowledges additional support from the Swiss Society of Friends of the Weizmann Institute of Science and S. S. H. acknowledges additional support from the Australian Research Council through Discovery Early Career Research Award No. DE150100315

Cathepsin B Acts as a Dominant Execution Protease in Tumor Cell Apoptosis Induced by Tumor Necrosis Factor

Death receptors can trigger cell demise dependent or independent of caspases. In WEHI-S fibrosarcoma cells, tumor necrosis factor (TNF) induced an increase in cytosolic cathepsin B activity followed by death with apoptotic features. Surprisingly, this process was enhanced by low, but effectively inhibiting, concentrations of pan-caspase inhibitors. Contrary to caspase inhibitors, a panel of pharmacological cathepsin B inhibitors, the endogenous cathepsin inhibitor cystatin A as well as antisense-mediated depletion of cathepsin B rescued WEHI-S cells from apoptosis triggered by TNF or TNF-related apoptosis-inducing ligand. Thus, cathepsin B can take over the role of the dominant execution protease in death receptor-induced apoptosis. The conservation of this alternative execution pathway was further examined in other tumor cell lines. Here, cathepsin B acted as an essential downstream mediator of TNF-triggered and caspase-initiated apoptosis cascade, whereas apoptosis of primary cells was only minimally dependent on cathepsin B. These data imply that cathepsin B, which is commonly overexpressed in human primary tumors, may have two opposing roles in malignancy, reducing it by its proapoptotic features and enhancing it by its known facilitation of invasion

Midkine is a NF-κB-inducible gene that supports prostate cancer cell survival

BackgroundMidkine is a heparin-binding growth factor that is over-expressed in various human cancers and plays important roles in cell transformation, growth, survival, migration, and angiogenesis. However, little is known about the upstream factors and signaling mechanisms that regulate midkine gene expression.MethodsTwo prostate cancer cell lines LNCaP and PC3 were studied for their expression of midkine. Induction of midkine expression in LNCaP cells by serum, growth factors and cytokines was determined by Western blot analysis and/or real-time quantitative reverse-transcription - polymerase chain reaction (RT-PCR). The cell viability was determined by the trypan blue exclusion assay when the LNCaP cells were treated with tumor necrosis factor alpha (TNFalpha) and/or recombinant midkine. When the LNCaP cells were treated with recombinant midkine, activation of intracellular signalling pathways was determined by Western blot analysis. Prostate tissue microarray slides containing 129 cases (18 normal prostate tissues, 40 early stage cancers, and 71 late stage cancers) were assessed for midkine expression by immunohistochemical staining.ResultsWe identified that fetal bovine serum, some growth factors (epidermal growth factor, androgen, insulin-like growth factor-I, and hepatocyte growth factor) and cytokines (TNFalpha and interleukin-1beta) induced midkine expression in a human prostate cancer cell line LNCaP cells. TNFalpha also induced midkine expression in PC3 cells. TNFalpha was the strongest inducer of midkine expression via nuclear factor-kappa B pathway. Midkine partially inhibited TNFalpha-induced apoptosis in LNCaP cells. Knockdown of endogenous midkine expression by small interfering RNA enhanced TNFalpha-induced apoptosis in LNCaP cells. Midkine activated extracellular signal-regulated kinase 1/2 and p38 mitogen-activated protein kinase pathways in LNCaP cells. Furthermore, midkine expression was significantly increased in late stage prostate cancer, which coincides with previously reported high serum levels of TNFalpha in advanced prostate cancer.ConclusionThese findings provide the first demonstration that midkine expression is induced by certain growth factors and cytokines, particularly TNFalpha, which offers new insight into understanding how midkine expression is increased in the late stage prostate cancer