Multi-Modal Traffic Simulation Calibration and Integration with Real-Time Hardware in Loop Simulator

The ongoing research in intelligent transport systems and connected and automated vehicles, enabled by advancements in artificial intelligence, integrating traffic simulations has become an essential part of product/software development for the automotive industry. Nowadays, traffic simulations are used to mimic real-world environment scenarios for virtual testing of advanced transportation technologies. With the increase in data collection methods for traffic flow, the calibration of the microscopic traffic simulations has emerged as an important research area. The underlying question in traffic modeling is how accurately simulations can mimic the real environment traffic flow conditions? This paper attempts to create a framework for microscopic traffic simulation calibration procedure which can be scaled for large networks. This paper makes the following major contributions. First, a calibration framework is proposed which harnesses the existing data set collected from The Ohio State University (OSU) campus bus service (CABS) busses using Global Positioning System (GPS) sensors to determine the traffic state in the real environment and create a microscopic traffic simulation. The traffic simulation is implemented for a section of the OSU campus (“Woody Hayes Drive") in an open-source traffic simulator – Simulation of Urban MObility (SUMO). The traffic flow generation is probabilistic to introduce variability between scenarios. The second contribution is the development of a communication interface between real-time dSpace ASM Hardware in Loop setup with SUMO to create a complete real-time simulation of urban environments for advanced driver assist systems (ADAS) virtual testing. Ademonstration scenario is the Ohio State University campus network with traffic demand generated using the calibrated model from the first part of the work

Заболевание тазобедренного сустава у детей с наследственной предрасположенностью: концептуальная модель

На основе принципов интегративной медицины, системного подхода с использованием концептуально−логического моделирования разработана единая система представлений о заболеваниях тазобедренного сустава у детей с наследственной предрасположенностью. Показано, что предлагаемый интегративный подход может служить основой для разработки диагностических и прогностических критериев развития суставов и проведения патогенетического хирургического лечения, направленного на ликвидацию или существенное снижение частоты формирования диспластического коксартроза.Based on the principles of integrative medicine, systemic approach with the use of concept of logical modelling, a uniform system of concepts about the diseases of the hip joint in children with hereditary susceptibility was worked out. It was shown that the suggested integrative approach can be used for working out diagnostic and prognostic criteria of joint development and performing pathogenetic surgery aimed at elimination or reduction in the frequency of forming dysplastic coxarthrosis

A phase 1b/pharmacokinetic trial of PTC299, a novel post-transcriptional VEGF inhibitor, for AIDS-related Kaposi’s sarcoma: AIDS Malignancy Consortium trial 059

Vascular endothelial growth factor (VEGF) plays an important role in Kaposi’s sarcoma (KS). We administered PTC299, a post-transcriptional inhibitor of pathogenic VEGF, to persons with HIV-related KS. Seventeen participants received three different doses of PTC299. Adverse events typically observed with VEGF-inhibition were absent. Three participants had partial tumor responses and 11 had stable disease. There were no differences in exposure to PTC299 by antiretroviral regimen. Serum VEGF, but not KSHV DNA, decreased on treatment. Given redundancies in the VEGF feedback loop, future trials should consider combining PTC299 with agents that inhibit different pathways implicated in KS and KSHV proliferation

The PI3K/Akt1 pathway enhances steady-state levels of FANCL

Fanconi anemia hematopoietic stem cells display poor self-renewal capacity when subjected to a variety of cellular stress. This phenotype raises the question of whether the Fanconi anemia proteins are stabilized or recruited as part of a stress response and protect against stem cell loss. Here we provide evidence that FANCL, the E3 ubiquitin ligase of the Fanconi anemia pathway, is constitutively targeted for degradation by the proteasome. We confirm biochemically that FANCL is polyubiquitinated with Lys-48-linked chains. Evaluation of a series of N-terminal-deletion mutants showed that FANCL's E2-like fold may direct ubiquitination. In addition, our studies showed that FANCL is stabilized in a complex with axin1 when glycogen synthase kinase-3β is overexpressed. This result leads us to investigate the potential regulation of FANCL by upstream signaling pathways known to regulate glycogen synthase kinase-3β. We report that constitutively active, myristoylated-Akt increases FANCL protein level by reducing polyubiquitination of FANCL. Two-dimensional PAGE analysis shows that acidic forms of FANCL, some of which are phospho-FANCL, are not subject to polyubiquitination. These results indicate that a signal transduction pathway involved in self-renewal and survival of hematopoietic stem cells also functions to stabilize FANCL and suggests that FANCL participates directly in support of stem cell function