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Open Access Publications from the University of California

Scholarly Works (6 results)

  • Thesis
  • Peer Reviewed
UCLA Electronic Theses and Dissertations (2023)

A proliferation of large active electronically-scanned arrays (AESA) is enabling precise beam steering in wireless communication links at millimeter wave carrier frequencies. In addition to radiated power, linear and nonlinear distortion from the transceivers and array elements must also be examined to discern their relative effects on received signal quality in the far field. For digital signals, error vector magnitude (EVM) represents a complete measure of the amplitude and phase distortion in a wireless channel. This work focuses on the analysis, simulation, and measurement of the EVM resulting from transmission by millimeter-wave antennas and phased arrays. An ultra-wideband (UWB) model of antenna transmission based on the vector effective length is presented and applied to EVM simulation of over-the-air (OTA) links for a microstrip patch and conical horn antenna at two different 5G FR2 bands. The EVM for the conical horn link is measured using a multi-port vector network analyzer (VNA) and compact antenna test range (CATR) provided by Keysight Technologies in Santa Rosa, CA. The same simulation and measurement techniques are then applied to analysis of phased array transmission to understand the effects of beam squint and embedded element frequency response. The EVM of individual active array element channels and the fully-active 8x8 phased array are measured as a function of RF carrier power, far field observation angles, beam scan angles, and modulation rates using MATLAB instrument control scripts. The feasibility of estimating the EVM of far field antenna links from the planar near fields (PNF) is also investigated. A theoretical framework for calculating EVM from wideband far fields derived through PNF transformations and results from PNF simulations and measurements of a Ka-band conical horn and 8x8 phased array are presented. Finally, the effective range of a vehicle-to-infrastructure antenna link at 5.9 GHz is estimated by calculating received power along a linear highway using the Friis free space transmission equation and full-wave simulations of base station and vehicular antenna arrays.

    Cover page: Characterization, Simulation, and Measurement of the Far Field Error Vector Magnitude of Millimeter-Wave Antennas and Phased Arrays using Compact and Planar Near Field Ranges
    • Article
    • Peer Reviewed
    UC San Diego Previously Published Works (2021)

    Background

    Non-invasive assessment of the hemodynamic changes of cirrhosis might help guide management of patients with liver disease but are currently limited.

    Purpose

    To determine whether free-breathing 4D flow MRI can be used to quantify the hemodynamic effects of cirrhosis and introduce hydraulic circuit indexes of severity.

    Study type

    Retrospective.

    Population

    Forty-seven patients including 26 with cirrhosis.

    Field strength/sequence

    3 T/free-breathing 4D flow MRI with soft gating and golden-angle view ordering.

    Assessment

    Measurements of the supra-celiac abdominal aorta, supra-renal abdominal aorta (SRA), celiac trunk (CeT), superior mesenteric artery (SMA), splenic artery (SpA), common hepatic artery (CHA), portal vein (PV), and supra-renal inferior vena cava (IVC) were made by two radiologists. Measures of hepatic vascular resistance (hepatic arterial relative resistance [HARR]; portal resistive index [PRI]) were proposed and calculated.

    Statistical analysis

    Bland-Altman, Pearson's correlation, Tukey's multiple comparison, and Cohen's kappa. P < 0.05 was considered significant.

    Results

    Forty-four of 47 studies yielded adequate image quality for flow quantification (94%). Arterial structures showed high inter-reader concordance (range; ρ = 0.948-0.987) and the IVC (ρ = 0.972), with moderate concordance in the PV (ρ = 0.866). Conservation of mass analysis showed concordance between large vessels (SRA vs. IVC; ρ = 0.806), small vessels (celiac vs. CHA + SpA; ρ = 0.939), and across capillary beds (CeT + SMA vs. PV; ρ = 0.862). Splanchnic flow was increased in patients with portosystemic shunting (PSS) relative to control patients and patients with cirrhosis without PSS (P < 0.05, difference range 0.11-0.68 liter/m). HARR was elevated and PRI was decreased in patients with PSS (3.55 and 1.49, respectively) compared to both the control (2.11/3.18) and non-PSS (2.11/2.35) cohorts.

    Data conclusion

    4D flow MRI with self-navigation was technically feasible, showing promise in quantifying the hemodynamic effects of cirrhosis. Proposed quantitative metrics of hepatic vascular resistance correlated with PSS.

    Level of evidence

    3 TECHNICAL EFFICACY STAGE: 2.
      Cover page: Quantification of the Hemodynamic Changes of Cirrhosis with Free‐Breathing Self‐Navigated MRI
      • Article
      • Peer Reviewed
      UC Davis Previously Published Works (2015)
      Cell death is a process of dying within biological cells that are ceasing to function. This process is essential in regulating organism development, tissue homeostasis, and to eliminate cells in the body that are irreparably damaged. In general, dysfunction in normal cellular death is tightly linked to cancer progression. Specifically, the up-regulation of pro-survival factors, including oncogenic factors and antiapoptotic signaling pathways, and the down-regulation of pro-apoptotic factors, including tumor suppressive factors, confers resistance to cell death in tumor cells, which supports the emergence of a fully immortalized cellular phenotype. This review considers the potential relevance of ubiquitous environmental chemical exposures that have been shown to disrupt key pathways and mechanisms associated with this sort of dysfunction. Specifically, bisphenol A, chlorothalonil, dibutyl phthalate, dichlorvos, lindane, linuron, methoxychlor and oxyfluorfen are discussed as prototypical chemical disruptors; as their effects relate to resistance to cell death, as constituents within environmental mixtures and as potential contributors to environmental carcinogenesis.
        Cover page: Disruptive environmental chemicals and cellular mechanisms that confer resistance to cell death.
        • Article
        • Peer Reviewed
        UC Davis Previously Published Works (2015)
        Cell death is a process of dying within biological cells that are ceasing to function. This process is essential in regulating organism development, tissue homeostasis, and to eliminate cells in the body that are irreparably damaged. In general, dysfunction in normal cellular death is tightly linked to cancer progression. Specifically, the up-regulation of pro-survival factors, including oncogenic factors and antiapoptotic signaling pathways, and the down-regulation of pro-apoptotic factors, including tumor suppressive factors, confers resistance to cell death in tumor cells, which supports the emergence of a fully immortalized cellular phenotype. This review considers the potential relevance of ubiquitous environmental chemical exposures that have been shown to disrupt key pathways and mechanisms associated with this sort of dysfunction. Specifically, bisphenol A, chlorothalonil, dibutyl phthalate, dichlorvos, lindane, linuron, methoxychlor and oxyfluorfen are discussed as prototypical chemical disruptors; as their effects relate to resistance to cell death, as constituents within environmental mixtures and as potential contributors to environmental carcinogenesis.
          Cover page: Disruptive environmental chemicals and cellular mechanisms that confer resistance to cell death
          • Article
          • Peer Reviewed
          UC San Francisco Previously Published Works (2015)
          Potentially carcinogenic compounds may cause cancer through direct DNA damage or through indirect cellular or physiological effects. To study possible carcinogens, the fields of endocrinology, genetics, epigenetics, medicine, environmental health, toxicology, pharmacology and oncology must be considered. Disruptive chemicals may also contribute to multiple stages of tumor development through effects on the tumor microenvironment. In turn, the tumor microenvironment consists of a complex interaction among blood vessels that feed the tumor, the extracellular matrix that provides structural and biochemical support, signaling molecules that send messages and soluble factors such as cytokines. The tumor microenvironment also consists of many host cellular effectors including multipotent stromal cells/mesenchymal stem cells, fibroblasts, endothelial cell precursors, antigen-presenting cells, lymphocytes and innate immune cells. Carcinogens can influence the tumor microenvironment through effects on epithelial cells, the most common origin of cancer, as well as on stromal cells, extracellular matrix components and immune cells. Here, we review how environmental exposures can perturb the tumor microenvironment. We suggest a role for disrupting chemicals such as nickel chloride, Bisphenol A, butyltins, methylmercury and paraquat as well as more traditional carcinogens, such as radiation, and pharmaceuticals, such as diabetes medications, in the disruption of the tumor microenvironment. Further studies interrogating the role of chemicals and their mixtures in dose-dependent effects on the tumor microenvironment could have important general mechanistic implications for the etiology and prevention of tumorigenesis.
            Cover page: The effect of environmental chemicals on the tumor microenvironment
            • Article
            • Peer Reviewed
            UC Davis Previously Published Works (2015)
            Lifestyle factors are responsible for a considerable portion of cancer incidence worldwide, but credible estimates from the World Health Organization and the International Agency for Research on Cancer (IARC) suggest that the fraction of cancers attributable to toxic environmental exposures is between 7% and 19%. To explore the hypothesis that low-dose exposures to mixtures of chemicals in the environment may be combining to contribute to environmental carcinogenesis, we reviewed 11 hallmark phenotypes of cancer, multiple priority target sites for disruption in each area and prototypical chemical disruptors for all targets, this included dose-response characterizations, evidence of low-dose effects and cross-hallmark effects for all targets and chemicals. In total, 85 examples of chemicals were reviewed for actions on key pathways/mechanisms related to carcinogenesis. Only 15% (13/85) were found to have evidence of a dose-response threshold, whereas 59% (50/85) exerted low-dose effects. No dose-response information was found for the remaining 26% (22/85). Our analysis suggests that the cumulative effects of individual (non-carcinogenic) chemicals acting on different pathways, and a variety of related systems, organs, tissues and cells could plausibly conspire to produce carcinogenic synergies. Additional basic research on carcinogenesis and research focused on low-dose effects of chemical mixtures needs to be rigorously pursued before the merits of this hypothesis can be further advanced. However, the structure of the World Health Organization International Programme on Chemical Safety 'Mode of Action' framework should be revisited as it has inherent weaknesses that are not fully aligned with our current understanding of cancer biology.
              Cover page: Assessing the carcinogenic potential of low-dose exposures to chemical mixtures in the environment: the challenge aheadCreative Commons 'BY-NC-ND' version 4.0 license
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