Runway exit designs for capacity improvement demonstrations. Phase 2: Computer model development

The development is described of a computer simulation/optimization model to: (1) estimate the optimal locations of existing and proposed runway turnoffs; and (2) estimate the geometric design requirements associated with newly developed high speed turnoffs. The model described, named REDIM 2.0, represents a stand alone application to be used by airport planners, designers, and researchers alike to estimate optimal turnoff locations. The main procedures are described in detail which are implemented in the software package and possible applications are illustrated when using 6 major runway scenarios. The main output of the computer program is the estimation of the weighted average runway occupancy time for a user defined aircraft population. Also, the location and geometric characteristics of each turnoff are provided to the user

Runway Exit Designs for Capacity Improvement Demonstrations. Phase 1: Algorithm Development

A description and results are presented of a study to locate and design rapid runway exits under realistic airport conditions. The study developed a PC-based computer simulation-optimization program called REDIM (runway exit design interactive model) to help future airport designers and planners to locate optimal exits under various airport conditions. The model addresses three sets of problems typically arising during runway exit design evaluations. These are the evaluations of existing runway configurations, addition of new rapid runway turnoffs, and the design of new runway facilities. The model is highly interactive and allows a quick estimation of the expected value of runway occupancy time. Aircraft populations and airport environmental conditions are among the multiple inputs to the model to execute a viable runway location and geometric design solution. The results presented suggest that possible reductions on runway occupancy time (ROT) can be achieved with the use of optimally tailored rapid runway designs for a given aircraft population. Reductions of up to 9 to 6 seconds are possible with the implementation of 30 m/sec variable geometry exits

Want to Make Your Website Better? Ask a Librarian.

Raise your hand if you have served on a committee in your library. If your hand isn’t raised, just give it some time … libraries definitely like committee work. For instance, I recently had the opportunity to work with a committee consisting mostly of librarians. When the committee’s goals were accomplished, my non-librarian coworker commented that “Librarians sure have a lot of opinions.” Since this article is about usability testing, and is written by and for librarians, let’s test his hypothesis. Let’s also test a few other hypotheses about librarians while we’re at it. (Disclaimer: In this article, “librarians” include staff who work in libraries, and has nothing to do with degrees or job classifications.) Washington County Cooperative Library Services (WCCLS) is a Cooperative of 13 member libraries and two special libraries, each uniquely governed and operated. WCCLS is a primary funding source for member libraries, and our WCCLS “Office” provides other support such as daily courier deliveries, cataloging coordination, and e-book collections. The WCCLS website and Extranet are two other ways the WCCLS Office supports member libraries in Washington County. The WCCLS Extranet is a repository of policies, procedures, and committee meeting documents. It also includes training and promotional materials for WCCLS resources, as well as opportunities for sharing ideas

Comparison of TRANSIMS' Light Duty Vehicle Emissions with On-Road Emission Measurements

The Transportation Analysis and Simulation System, TRANSIMS, contains a vehicle emissions module that estimates tailpipe emissions for light and heavy-duty vehicles and evaporative emissions for light-duty vehicles. This paper describes and validates the TRANSIMS emission module and compares its emission estimates to on-road emission-measurements and other state-of-the-art emission models. The trend of the emissions estimated in thirteen different runs in each model are compared. The results indicate that the TRANSIMS model provides consistent trends of estimated carbon monoxide (CO) and hydrocarbons (HC) with field data trends and inconsistent trends of estimated nitrogen lxides (NOx). However, the magnitude of the emission estimated in TRANSIMS is closer to the field data than for other models

Imaging features of histological subtypes of hepatocellular carcinoma: Implication for LI-RADS

Background & Aims: The histopathological subtypes of hepatocellular carcinoma (HCC) are associated with distinct clinical features and prognoses. This study aims to report Liver Imaging Reporting and Data System (LI-RADS)-defined imaging features of different HCC subtypes in a cohort of resected tumours and to assess the influence of HCC subtypes on computed tomography (CT)/magnetic resonance imaging (MRI) LI-RADS categorisation in the subgroup of high-risk patients.Methods: This retrospective institutional review board-approved study included patients with resected HCCs and available histopathological classification. Three radiologists independently reviewed preoperative CT and MRI exams. The readers evaluated the presence of imaging features according to LI-RADS v2018 definitions and provided a LI-RADS category in patients at high risk of HCC. Differences in LI-RADS features and categorisations were assessed for not otherwise specified (NOS-HCC), steatohepatitic (SH-HCC), and macrotrabecular-massive (MTM-HCC) types of HCCs.Results: Two hundred and seventy-seven patients (median age 64.0 years, 215 [77.6%] men) were analysed, which involved 295 HCCs. There were 197 (66.7%) NOS-HCCs, 62 (21.0%) SH-HCCs, 23 (7.8%) MTM-HCCs, and 13 (4.5%) other rare subtypes. The following features were more frequent in MTM-HCC: elevated alpha-foetoprotein serum levels (p <0.001), tumour-in-vein (p <0.001 on CT, p <= 0.052 on MRI), presence of at least 1 LR-M feature (p <= 0.010 on CT), infiltrative appearance (p <= 0.032 on CT), necrosis or severe ischaemia (p <= 0.038 on CT), and larger size (p <= 0.006 on CT, p <= 0.011 on MRI). SH-HCC was associated with fat in mass (p <0.001 on CT, p <= 0.002 on MRI). The distribution of the LI-RADS major features and categories in high-risk patients did not significantly differ among the 3 main HCC subtypes.Conclusions: The distribution of LI-RADS major features and categories is not different among the HCC subtypes. Nevertheless, careful analysis of tumour-in-vein, LR-M, and ancillary features as well as clinico-biological data can provide information for the non-invasive diagnosis of HCC subtypes.Lay summary: In high-risk patients, the overall distribution of LI-RADS major features and categories is not different among the histological subtypes of hepatocellular carcinoma, but tumour-in-vein, presence of LR-M features, and ancillary features can provide information for the non-invasive diagnosis of hepatocellular carcinoma subtypes. (C) 2021 The Authors. Published by Elsevier B.V. on behalf of European Association for the Study of the Liver (EASL)

Kidins220/ARMS binds to the B cell antigen receptor and regulates B cell development and activation

B cell antigen receptor (BCR) signaling is critical for B cell development and activation. Using mass spectrometry, we identified a protein kinase D\u2013interacting substrate of 220 kD (Kidins220)/ankyrin repeat\u2013rich membrane-spanning protein (ARMS) as a novel interaction partner of resting and stimulated BCR. Upon BCR stimulation, the interaction increases in a Src kinase\u2013independent manner. By knocking down Kidins220 in a B cell line and generating a conditional B cell\u2013specific Kidins220 knockout (B-KO) mouse strain, we show that Kidins220 couples the BCR to PLC\u3b32, Ca2+, and extracellular signal-regulated kinase (Erk) signaling. Consequently, BCR-mediated B cell activation was reduced in vitro and in vivo upon Kidins220 deletion. Furthermore, B cell development was impaired at stages where pre-BCR or BCR signaling is required. Most strikingly, \u3bb light chain\u2013positive B cells were reduced sixfold in the B-KO mice, genetically placing Kidins220 in the PLC\u3b32 pathway. Thus, our data indicate that Kidins220 positively regulates pre-BCR and BCR functionin

B cell antigen receptor expression and phosphatidylinositol 3-kinase signaling regulate genesis and maintenance of mouse chronic lymphocytic leukemia

Chronic lymphocytic leukemia (CLL) is a frequent lymphoproliferative disorder of B cells. Although inhibitors targeting signal proteins involved in B cell antigen receptor (BCR) signaling constitute an important part of the current therapeutic protocols for CLL patients, the exact role of BCR signaling, as compared to genetic aberration, in the development and progression of CLL is controversial. To investigate whether BCR expression per se is pivotal for the development and maintenance of CLL B cells, we used the TCL1 mouse model. By ablating the BCR in CLL cells from TCL1 transgenic mice, we show that CLL cells cannot survive without BCR signaling and are lost within eight weeks in diseased mice. Furthermore, we tested whether mutations augmenting B cell signaling influence the course of CLL development and its severity. The Phosphatidylinositol-3-kinase (PI3K) signaling pathway is an integral part of the BCR signaling machinery and its activity is indispensable for B cell survival. It is negatively regulated by the lipid phosphatase PTEN, whose loss mimics PI3K pathway activation. Herein, we show that PTEN has a key regulatory function in the development of CLL, as deletion of the Pten gene resulted in greatly accelerated onset of the disease. By contrast, deletion of the gene TP53, which encodes the tumor suppressor p53 and is highly mutated in CLL, did not accelerate disease development, confirming that development of CLL was specifically triggered by augmented PI3K activity through loss of PTEN and suggesting that CLL driver consequences most likely affect BCR signaling. Moreover, we could show that in human CLL patient samples, 64% and 81% of CLL patients with a mutated and unmutated IgH VH, respectively, show downregulated PTEN protein expression in CLL B cells if compared to healthy donor B cells. Importantly, we found that B cells derived from CLL patients had higher expression levels of the miRNA-21 and miRNA-29, which suppresses PTEN translation, compared to healthy donors. The high levels of miRNA-29 might be induced by increased PAX5 expression of the B-CLL cells. We hypothesize that downregulation of PTEN by increased expression levels of miR-21, PAX5 and miR-29 could be a novel mechanism of CLL tumorigenesis that is not established yet. Together, our study demonstrates the pivotal role for BCR signaling in CLL development and deepens our understanding of the molecular mechanisms underlying the genesis of CLL and for the development of new treatment strategies

PROviding Better ACcess To ORgans: A comprehensive overview of organ‐access initiatives from the ASTS PROACTOR Task Force

Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/138905/1/ajt14441_am.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/138905/2/ajt14441.pd