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Introduction To identify the effect of Obstructive Sleep Apnea (OSA) and sleep duration on problems with health-related quality of life (HR-QoL) in children. Methods Children ages 8–18 years visiting sleep laboratory from 07/2019 to 01/2020 for overnight PSG participated in the study. Controls seen during 01/2020-02/2020 for issues other than sleep disturbance were recruited from the primary care pediatric clinics. HR-QoL was assessed by PROMIS V1.0 questionnaires. Statistical analysis was conducted using R 3.6.0. Results 122 children were studied: 64 males (52.4%).Twenty-nine(29.2%) had mild OSA, 8 (8.1%) moderate OSA, 17 (17.1%) severe OSA,46 (46.4%) were diagnosed with No-OSA and 22 (18.0%) were controls. Patients visiting the sleep laboratory had lower physical function mobility compared to controls (p=0.004). With increasing severity of OSA, there was a step wise decrease in physical function mobility (p=0.01). Correlation analysis suggested that physical function mobility was positively associated with total sleep duration (p=0.02) and negatively associated with apnea hypopnea index (p=0.01). Symptoms of anxiety in children was positively associated with number of arousals (p=0.04). Age was positively associated with fatigue (p=0.02) and negatively associated with deep sleep (p Conclusion We found interrupted sleep associated with symptoms of anxiety. OSA and reduced sleep duration are associated with problems with physical function mobility after adjusting for age, gender and number of arousals. Support (if any) None

Introduction To identify the status of health-related quality of life (HR-QoL) domains in children with sleep disturbance. Methods Patients ages 5–17 years visiting sleep laboratory from 09/2019 to 01/2020 for overnight PSG participated in the study. Age and sex matched control participants were seen in general pediatrics during 02/2020 for issues other than sleep disturbance. HR-QoL was assessed by PROMIS V1.0 questionnaires. Statistical analysis was conducted using R 3.6.0. Results 122 patients were included in the final analysis: 70 males (57.4%). Ninety nine (81.15%) patients were included from the sleep laboratory and 23 (18.85%) controls were recruited from the department of pediatrics. Among the patients visiting sleep laboratory, thirty one (25.4%) had mild OSA, 12 (9.8%) moderate OSA, 19 (15.6%) severe OSA, 37 (30.3%) were diagnosed with No-OSA. Twenty three (18.9%) controls were visiting to the hospital for their routine wellness examination requiring no PSG. Severity of OSA was not correlated with any HR-QoL domain. Patients visiting the sleep laboratory had lower life satisfaction (p=0.05) and higher physical stress experience (p=0.005). Age, BMI were negatively and N3 sleep was positively associated with family relations (p Conclusion Children visiting sleep laboratory had higher physical stress experience and lower life satisfaction as compared to controls. Deep sleep was associated with problems with family relations, life satisfaction and anger. Regression analysis suggested that age was negatively associated with family relations and life satisfaction. Support (if any) None

Natural gas vehicles (NGV) have attracted more and more attention from policy makers since natural gas is a clean substitute for traditional fossil fuel that is also readily accessible. In some areas such as the state of Texas, vehicles that do not use traditional fossil fuel (e.g., NGVs) are exempt from paying fuel taxes. Government financial incentives have motivated substantial adoption of NGVs. This paper studies NGV adoption behavior in both U.S. and Texas markets to estimate the dynamics of NGV diffusion. This research employs well-known Bass diffusion models applied to NGV adoption, using data from both the U.S. and Texas. Among several interesting results, we find that NGV adoption through an imitation effect appears to be significant for the U.S. NGV market.

This paper introduces a novel information hiding technique for Flash memory. The method hides data within an analog characteristic of Flash, the program time of individual bits. Because the technique uses analog behaviors, normal Flash memory operations are not affected and hidden information is invisible in the data stored in the memory. Even if an attacker checks a Flash chip's analog characteristics, experimental results indicate that the hidden information is difficult to distinguish from inherent manufacturing variation or normal wear on the device. Moreover, the hidden data can survive erasure of the Flash memory data, and the technique can be used on current Flash chips without hardware changes.

This paper presents a new nonvolatile SRAM design that incorporates low-voltage nanocrystal PMOS Flash transistors. The design enables global store, restore and erase operations with negligible penalty on regular SRAM operation. Store/erase operations also do not consume much power even considering charge pump circuits. Circuit simulations based on experimental I–V characteristics demonstrate that 10 µs store/erase operation at ± 6 Vis sufficient for correct restoration of the stored bit even under reasonable process variation.

This paper presents a model-assisted routing technique for improving lithography robustness of synthesized layouts. Presupposing an accurate lithography model and a model-based layout weak spot identification procedure, this method produces routed layout in-situ with acceptable turn around time. The approach starts with a conventionally routed layout that, although conforming to design rules, may contain undesirable layout configurations that the router should reconcile. Since weak spot identification is computation intensive, rule-based filtering is first applied to the incoming layout to select regions for further model-based analysis. The router then performs a non-discriminate correction to reduce the number of potential weak spots. This reduced set subsequently undergoes model-based weak spot analysis, distinguishing the actual weak spots. The router finally optimizes the layout to remove the identified weak spots. This technique has been implemented in an industry detail router, and tested with 65-nm technology. Experimental results show that this method can effectively remove actual weak spots with reasonable runtime.

This paper reports the device process and reliability aspects of a high voltage InGaP/GaAs HBT technology for 28V operation. The key differences and challenges from the material and process perspectives relative to the conventional low voltage HBT technology are first described. Long-term reliability tests performed at 28V bias voltage, 5.2kA/cm2 current density and 310degC junction temperature resulted in zero device failures after over 3600 hours of stress. Wafer-level reliability tests using extreme current stress conditions were used to force transistors to degrade in short time for quick checking of transistor integrity and process reliability. Transistor lifetimes were generally higher than those in conventional low voltage HBTs at similar junction temperatures. Combining with the previously reported ruggedness and linearity performance, the high voltage InGaP/GaAs HBT is a mature technology for use in the 28V high linearity power amplification

Tumor hypoxia is associated with disease progression, drug resistance and poor prognosis. It has been shown previously that hypoxia prolongs the activation of epidermal growth factor receptor (EGFR) by delaying clathrin-dependent endocytosis-mediated deactivation of receptors. Recently, caveolin (CAV) mediated signaling and trafficking have been reported to be involved in the oncogenesis of many tumours, including clear cell renal cell carcinoma (CCRCC). However, the role of CAV-1 in the tumor progression is unclear. Here, we show that the loss of von Hippel-Lindau (VHL) protein – the principal negative regulator of hypoxia-inducible factor (HIF) – increases the auto-phosphorylation of epidermal growth factor receptor (EGFR), thus attributing to an enhanced ligand-independent cell signaling pathway, majorly Ras-Raf-MEK-ERK pathway, and leading to cell proliferation. The auto-phosphorylation of EGFR is due to the HIF-dependent overexpression of caveolin-1 (CAV-1) at the level of transcription, which enhances the association between EGFR and CAV-1 and the auto-dimerization of EGFR. Primary CCRCC tumors and numerous hypoxia treated tumor cell lines exhibit significantly higher expression of CAV-1 protein. Using a dorsal skin-fold window chamber on SCID mice, shCAV-1 knockdown 786-O tumor cell line exhibits lower growth than that of shscramble counterpart in xenografts. These findings support a model in which tumour hypoxia or oncogenic activation of HIF prolongs ligand-independent RTK signaling through the over-expression of CAV-1. Given the oncogenic role of CAV-1, it should be considered as a future therapeutic target in cancer treatment. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 1973. doi:10.1158/1538-7445.AM2011-1973

Caveolin-1 (Cav-1) is a multifunctional scaffolding protein with multiple binding partners that is associated with cell surface caveolae and the regulation of lipid raft domains. Cav-1 regulates multiple cancer-associated processes including cellular transformation, tumour growth, cell death and survival, and multidrug resistance. A high expression of Cav-1 is found in various cancer , including clear cell renal cell carcinoma (CCRCC), correlating with large, high grade tumors and poor prognosis. However, the role of Cav-1 in the oncogenesis of CCRCC remains unclear, and its role as either an oncogene or tumour suppressor is still under debate. Here, we investigated the mechanism of Cav-1 in controlling cell proliferation using in vitro and in vivo assays. We report that Cav-1 is highly expressed in tumour compared to normal tissue in patients with CCRCC, thus Cav-1 likely functions as an oncogene. Upon knock-down of Cav-1, tumour cells (786-VHL-/-) showed a decrease in proliferation. We showed that Cav-1 is associating with EGFR, a receptor tyrosine kinase, to activate the Ras-RAF-MEK-ERK kinase pathway and induce cell proliferation. We found that Cav-1 binds to EGFR in immunoprecipitation. The Ras pathway is upregulated in cells overexpressing Cav-1 after EGF stimulation. Upon knockdown of Cav-1, the level of p-ERK, p-MEK, and p-c-Raf decreased, as well as the rate of cell proliferation. Upstream of the Ras pathway, we report that Cav-1 appears to be under the control of hypoxia-inducible factor (HIF). Under hypoxia, VHL (the principal negative regulator of HIF) is downregulated, thus leading to upregulation of HIF. We showed that under hypoxia, Cav-1 increased in 786-VHL, Hela and A431 cell lines. Similarly, cells with VHL loss (786-VHL-/-), thus high HIF level, had high levels of Cav-1. We are currently examining the role of Cav-1 in tumour growth by injecting SCID mice with either 786-VHL-/-, or Cav-1 knock-down 786-VHL-/- tumour cells. Since Cav-1 level seems to be under the control of HIF in renal, cervical and squamous carcinoma cell lines, it suggests that the oxygen sensing pathway plays a general role in controlling cell proliferation through upregulating Cav-1. Cav-1 should be considered as a target for drug design as the knock down of Cav-1 decreased cell proliferation and could potentially decrease tumour growth. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 459.