Comparative Study Between Software Tools Help Deluxe Pc Version 5.5 and Norton Utilities Version 4.5 Advanced Edition

Number of issues arising in connection with the efficiency and maintenance of a file / disk atlarge, and the development of computer technology along with its software, causing the softwarecan not be excluded anymore. Because so many types of assistive software available, in thispaper focuses on two research software that is very popular in Indonesia, namely PC ToolsDeluxe Version 5.5 and Norton Utilities Advanced Edition Version 4.5. Activities includesurveys and interviews conducted with several users who have enough experience in the use ofboth the software earlier. After obtaining the problem, gathered the abilities possessed by each ofthe software and compared. From the comparison results can be perceived advantages anddisadvantages of each, and should be used is unknown when Toos PC Deluxe 5.5 and when usedNorton Utilities Advanced Edition 4.5

Rate of Convergence Towards Hartree Dynamics

We consider a system of N bosons interacting through a two-body potential with, possibly, Coulomb-type singularities. We show that the difference between the many-body Schr\"odinger evolution in the mean-field regime and the effective nonlinear Hartree dynamics is at most of the order 1/N, for any fixed time. The N-dependence of the bound is optimal.Comment: 26 page

Rate of Convergence Towards Semi-Relativistic Hartree Dynamics

We consider the semi-relativistic system of $N$ gravitating Bosons with gravitation constant $G$. The time evolution of the system is described by the relativistic dispersion law, and we assume the mean-field scaling of the interaction where $N \to \infty$ and $G \to 0$ while $GN = \lambda$ fixed. In the super-critical regime of large $\lambda$, we introduce the regularized interaction where the cutoff vanishes as $N \to \infty$. We show that the difference between the many-body semi-relativistic Schr\"{o}dinger dynamics and the corresponding semi-relativistic Hartree dynamics is at most of order $N^{-1}$ for all $\lambda$, i.e., the result covers the sub-critical regime and the super-critical regime. The $N$ dependence of the bound is optimal.Comment: 29 page

Flagellate dermatitis following consumption of shiitake mushroom

Japanese dermatologists were the first to describe the very characteristic flagellate dermatitis following consumption of under-cooked or raw shiitake mushroom (Lentinus edodes). These similar eruptions were also reported in patients treated with bleomycin, in dermatomyositis and adult onset Still’s disease. We report a case where a 40 year old chinese female developed flagellate dermatitis following ingestion of a bun containing shiitake mushroom

Role of Delta-like 4 in Jagged1-induced tumour angiogenesis and tumour growth

Delta-like 4 (DLL4) and Jagged1 (JAG1) are two key Notch ligands implicated in tumour angiogenesis. They were shown to have opposite effects on mouse retinal and adult regenerative angiogenesis. In tumours, both ligands are upregulated but their relative effects and interactions in tumour biology, particularly in tumour response to therapeutic intervention are unclear. Here we demonstrate that DLL4 and JAG1 displayed equal potency in stimulating Notch target genes in HMEC-1 endothelial cells but had opposing effects on sprouting angiogenesis in vitro. Mouse DLL4 or JAG1 expressed in glioblastoma cells decreased tumour cell proliferation in vitro but promoted tumour growth in vivo. mDLL4-expressing tumours showed fewer but larger vessels whereas mJAG1-tumours produced more vessels. In both tumour types pericyte coverage was decreased but the vessels were more perfused. Both ligands increased tumour resistance towards anti-VEGF therapy but the resistance was higher in mDLL4-tumours versus mJAG1-tumours. However, their sensitivity to the therapy was restored by blocking Notch signalling with dibenzazepine. Importantly, anti-DLL4 antibody blocked the effect of JAG1 on tumour growth and increased vessel branching in vivo. The mechanism behind the differential responsiveness was due to a positive feedback loop for DLL4-Notch signalling, rendering DLL4 more dominant in activating Notch signalling in the tumour microenvironment. We concluded that DLL4 and JAG1 promote tumour growth by modulating tumour angiogenesis via different mechanisms. JAG1 is not antagonistic but utilises DLL4 in tumour angiogenesis. The results suggest that anti-JAG1 therapy should be explored in conjunction with anti-DLL4 treatment in developing anti-Notch therapies in clinics

Management of severe hidradenitis suppurativa with biologic therapy and wide excision

Hidradenitis suppurativa (HS) is a chronic inflammatory follicular occlusive disease that involves the intertriginous areas. Treatment methods include conventional topical and systemic medication, radiotherapy, biologic agents, and surgical excision. Of late, there has been an increased focus on the use of biologic agents in patients with moderate to severe HS. Here, we present the case of a 46-year-old man with Hurley stage III HS for whom wide excision was ultimately curative, after aggressive medical therapy with the use of infliximab and adalimumab had succeeded in limiting the body surface area affected by the disease. This case demonstrates the effective treatment of severe HS with a combination of biologic therapy and surgery

DLL4-Notch Signaling Mediates Tumor Resistance to Anti-VEGF Therapy \u3ci\u3eIn Vivo\u3c/i\u3e

Resistance to VEGF inhibitors is emerging as a major clinical problem. Notch signaling has been implicated in tumor angiogenesis. Therefore, to investigate mechanisms of resistance to angiogenesis inhibitors, we transduced human glioblastoma cells with retroviruses encoding Notch delta-like ligand 4 (DLL4), grew them as tumor xenografts and then treated the murine hosts with the VEGF-A inhibitor bevacizumab. We found that DLL4-mediated tumor resistance to bevacizumab in vivo. The large vessels induced by DLL4-Notch signaling increased tumor blood supply and were insensitive to bevacizumab. However, blockade of Notch signaling by dibenzazepine, a ?-secretase inhibitor, disrupted the large vessels and abolished the tumor resistance. Multiple molecular mechanisms of resistance were shown, including decreased levels of hypoxia-induced VEGF and increased levels of the VEGF receptor VEGFR1 in the tumor stroma, decreased levels of VEGFR2 in large blood vessels, and reduced levels of VEGFR3 overall. DLL4-expressing tumors were also resistant to a VEGFR targeting multikinase inhibitor. We also observed activation of other pathways of tumor resistance driven by DLL4-Notch signaling, including the FGF2-FGFR and EphB4-EprinB2 pathways, the inhibition of which reversed tumor resistance partially. Taken together, our findings show the importance of classifying mechanisms involved in angiogenesis in tumors, and how combination therapy to block DLL4-Notch signaling may enhance the efficacy of VEGF inhibitors, particularly in DLL4-upregulated tumors, and thus provide a rational base for the development of novel strategies to overcome antiangiogenic resistance in the clinic. Cancer Res; 71(18); 6073–83. ©2011 AACR