Development of software for computing forming information using a component based approach

ABSTRACTIn shipbuilding industry, the manufacturing technology has advanced at an unprecedented pace for the last decade. As a result, many automatic systems for cutting, welding, etc. have been developed and employed in the manufacturing process and accordingly the productivity has been increased drastically. Despite such improvement in the manufacturing technology, however, development of an automatic system for fabricating a curved hull plate remains at the beginning stage since hardware and software for the automation of the curved hull fabrication process should be developed differently depending on the dimensions of plates, forming methods and manufacturing processes of each shipyard. To deal with this problem, it is necessary to create a “plug-in” framework, which can adopt various kinds of hardware and software to construct a full automatic fabrication system. In this paper, a framework for automatic fabrication of curved hull plates is proposed, which consists of four components and related software. In particular the software module for computing fabrication information is developed by using the ooCBD development methodology, which can interface with other hardware and software with minimum effort. Examples of the proposed framework applied to medium and large shipyards are presented

New Precision Electroweak Tests in Supergravity Models

We update the analysis of the precision electroweak tests in terms of 4 epsilon parameters, $\epsilon_{1,2,3,b}$, to obtain more accurate experimental values of them by taking into account the new LEP data released at the 28th ICHEP (1996, Poland). We also compute $\epsilon_1$ and $\epsilon_b$ in the context of the no-scale $SU(5)\times U(1)$ supergravity model to obtain the updated constraints by imposing the correlated constraints in terms of the experimental ellipses in the $\epsilon_1-\epsilon_b$ plane and also by imposing the new bound on the lightest chargino mass, $m_{\chi^\pm_1}\gtrsim 79$ $GeV$. Upon imposing these new experimental results, we find that the situations in the no-scale model are much more favorable than those in the standard model, and if $m_t\gtrsim 170$ $GeV$, then the allowed regions at the 95% C.~L. in the no-scale model are $\tan\beta\gtrsim 4$ and $m_{\chi^\pm_1}\lesssim 120 (82)$ $GeV$ for $\mu>0 (\mu<0)$, which are in fact much more stringent than in our previous analysis. Therefore, assuming that $m_t\gtrsim 170$ $GeV$, if the lightest chargino mass bound were to be pushed up only by a few GeV, the sign on the Higgs mixing term $\mu$ in the no-scale model could well be determined from the $\epsilon_1-\epsilon_b$ constraint to be positive at the 95% C.~L. At any rate, better accuracy in the measured $m_t$ from the Tevatron in the near future combined with the LEP data is most likely to provide a decisive test of the no-scale $SU(5)\times U(1)$ supergravity model.Comment: 15 pages, REVTEX, 1 figure (not included but available as a ps file from [email protected]

High Grade Hemangioendothelioma of the Temporal Bone in a Child: A Case Report

Hemangioendothelioma is a rare vascular tumor characterized by endothelial tumor cells and variable malignant behavior, and it's not common for this lesion to involve the bone. Although there are a few reports of cranial involvement by hemangioendothelioma, only rare cases arising in temporal bone have been published. We present the radiologic findings of a 7-year-old boy who had a high grade hemangioendothelioma involving the temporal bone with intracranial extension. Evidence of flow voids on MR images suggested a tumor of vascular origin, and the ill-defined margins, cortical destruction and intracranial extension on the CT and MR images were correlated with the tumor's high histologic grade

A Case of Familial Comedonal Darier's Disease

Darier's disease is a genetic disorder of keratinization with autosomal dominant inheritance. Its appearance is usually in the form of greasy, crusted, keratotic yellow-brown papules and plaques found particularly on seborrheic areas of the body. However, there are some clinical variants showing atypical skin lesions. Here we report an unusual case of Darier's disease, which mainly showed prominent comedonal papules over the face

Targeting ETosis by miR-155 inhibition mitigates mixed granulocytic asthmatic lung inflammation

Asthma is phenotypically heterogeneous with several distinctive pathological mechanistic pathways. Previous studies indicate that neutrophilic asthma has a poor response to standard asthma treatments comprising inhaled corticosteroids. Therefore, it is important to identify critical factors that contribute to increased numbers of neutrophils in asthma patients whose symptoms are poorly controlled by conventional therapy. Leukocytes release chromatin fibers, referred to as extracellular traps (ETs) consisting of double-stranded (ds) DNA, histones, and granule contents. Excessive components of ETs contribute to the pathophysiology of asthma; however, it is unclear how ETs drive asthma phenotypes and whether they could be a potential therapeutic target. We employed a mouse model of severe asthma that recapitulates the intricate immune responses of neutrophilic and eosinophilic airway inflammation identified in patients with severe asthma. We used both a pharmacologic approach using miR-155 inhibitor-laden exosomes and genetic approaches using miR-155 knockout mice. Our data show that ETs are present in the bronchoalveolar lavage fluid of patients with mild asthma subjected to experimental subsegmental bronchoprovocation to an allergen and a severe asthma mouse model, which resembles the complex immune responses identified in severe human asthma. Furthermore, we show that miR-155 contributes to the extracellular release of dsDNA, which exacerbates allergic lung inflammation, and the inhibition of miR-155 results in therapeutic benefit in severe asthma mice. Our findings show that targeting dsDNA release represents an attractive therapeutic target for mitigating neutrophilic asthma phenotype, which is clinically refractory to standard care

Novel Peptide Nanoparticle Biased Antagonist of CCR3 Blocks Eosinophil Recruitment and Airway Hyperresponsiveness

Background—Chemokine signaling through CCR3 is a key regulatory pathway for eosinophil recruitment into tissues associated with allergic inflammation and asthma. To date, none of the CCR3 antagonists have shown efficacy in clinical trials. One reason may be their unbiased mode of inhibition that prevents receptor internalization, leading to drug tolerance. Objective—We sought to develop a novel peptide nanoparticle CCR3 inhibitor (R321) with a biased mode of inhibition that would block G-protein signaling, but enable or promote receptor internalization. Methods—Self-assembly of R321 peptide into nanoparticles and peptide binding to CCR3 were analyzed by dynamic light scattering and NMR. Inhibitory activity on CCR3 signaling was assessed in vitro using flow cytometry, confocal microscopy, and western blot analysis in a CCR3+ eosinophil cell line and blood eosinophils. In vivo effects of R321 were assessed using a triple allergen mouse asthma model. Results—R321 self-assembles into nanoparticles and binds directly to CCR3, altering receptor function. IC50 values for eotaxin-induced chemotaxis of blood eosinophils are in the low nanomolar range. R321 inhibits only the early phase of ERK1/2 activation and not the late phase generally associated with β-arrestin recruitment and receptor endocytosis, promoting CCR3 internalization and degradation. In vivo, R321 effectively blocks eosinophil recruitment into the lungs and airways and prevents airway hyperresponsiveness in a mouse eosinophilic asthma model. Conclusions—R321 is a potent and selective antagonist of the CCR3 signaling cascade. Inhibition through a biased mode of antagonism may hold significant therapeutic promise by eluding the formation of drug tolerance

Sublingual Immunization with a Live Attenuated Influenza A Virus Lacking the Nonstructural Protein 1 Induces Broad Protective Immunity in Mice

The nonstructural protein 1 (NS1) of influenza A virus (IAV) enables the virus to disarm the host cell type 1 IFN defense system. Mutation or deletion of the NS1 gene leads to attenuation of the virus and enhances host antiviral response making such live-attenuated influenza viruses attractive vaccine candidates. Sublingual (SL) immunization with live influenza virus has been found to be safe and effective for inducing protective immune responses in mucosal and systemic compartments. Here we demonstrate that SL immunization with NS1 deleted IAV (DeltaNS1 H1N1 or DeltaNS1 H5N1) induced protection against challenge with homologous as well as heterosubtypic influenza viruses. Protection was comparable with that induced by intranasal (IN) immunization and was associated with high levels of virus-specific antibodies (Abs). SL immunization with DeltaNS1 virus induced broad Ab responses in mucosal and systemic compartments and stimulated immune cells in mucosa-associated and systemic lymphoid organs. Thus, SL immunization with DeltaNS1 offers a novel potential vaccination strategy for the control of influenza outbreaks including pandemics