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Open Access Publications from the University of California

Scholarly Works (94 results)

  • Multimedia
CMPM 80K (2019)
I choose the word 'traffic ' for my theme. All events are happening on a train, which is a form of traffic. I wanted the player to feel claustrophobic. The train is a closed space. You cannot escape the situation inside unless it stops at any station. SPOILER: I wanted the player to explore various endings, including the haunting hidden ending.
  • 13 supplemental images
  • 1 supplemental file
Creative Commons 'BY-NC' version 4.0 license
  • Thesis
  • Peer Reviewed
UC San Diego Electronic Theses and Dissertations (2012)
This thesis demonstrates the silicon-based on-chip W-band phased array systems. An improved wideband I/Q network to minimize the capacitive loading problem is presented, and its implementation in a 60-80 GHz active phase shifter using 0.13 [mu]m SiGe BiCMOS process is demonstrated. In addition, a 67-78 GHz 4-bit passive phase shifter using low-pass pi-network and 0.13 [mu]m CMOS switches is demonstrated. By adding amplifiers to the passive phase shifter with the architecture of alternating amplifiers and phase shifter cells, a low-power BiCMOS 4-element phased array receiver for 76-84 GHz applications are presented. Lastly, a 76-84 GHz 16-element phased array receiver, designed differentially in order to reduce the sensitivity to packaging effect such as ground inductance, is presented. This thesis presents the silicon-based on- chip W-band phased array systems. An improved quadrature all-pass filter (QAF) and its implementation in 60-80 GHz active phase shifter using 0.13 [mu]m SiGe BiCMOS technology is presented. It is demonstrated that with the inclusion of an Rs/R in the high Q branches of C and L, the sensitivity to the loading capacitance, therefore the I/Q phase and amplitude errors are minimized. This technique is especially suited for wideband millimeter- wave circuits where the loading capacitance (CL) is comparable to the filter capacitance (C). A prototype 60- 80 GHz active phased shifter using the improved QAF is demonstrated. The overall chip size is 1.15 x 0.92 mm² with the power consumption of 108 mW. The measured S₁1 and S₂2 are < -10 dB at 60-80 GHz and 60-73 GHz, respectively. The measured average power gain is 11.0-14.7 dB at 60-79 GHz with the rms gain error of < 1.3 dB at 60-78 GHz for 4 -bit phase states. And the rms phase error is < 9.1° at 60-78.5 GHz showing wideband 4-bit performance. The measured NF is 9-11.6 dB at 63-75 GHz and the measured P₁dB is -27 dBm at 70 GHz. In another project, a 67-78 GHz 4-bit passive phase shifter using 0.13 um CMOS switches is demonstrated. The phase shifter is based on a low-pass pi- network. The chip size is 0.45 x 0.3 mm² without pads and consumes virtually no power. The measured S₁1 and S₂2 is < -10 dB at 67-81 GHz for all 16 phase states. The measured gain of 4-bit phase shifter is -19.2 +/- 3.7 dB at 77 GHz with the rms gain error of < 11.25° at 67-78 GHz. And the measured rms phase error is < 2.5 dB at 67-78 GHz. The measured P1dB is > 8 dBm and the simulated IIP3 is > 22 dBm. A low-power 76--84 GHz 4-element phased array receiver using the designed passive phase shifter is presented. The power consumption is minimized by using a single-ended design and alternating the amplifiers and phase shifter cells to result in a low noise figure at a low power consumption. A variable gain amplifier and the 11 degree phase shifter are used to correct for the rms gain and phase errors at different operating frequencies. The overall chip size is 2.0 x 2.7 mm² with the current consumption of 18 mA/channel with 1.8 V supply voltage. The measured S₁1 and S²2 is < -10 dB at 70-88 GHz and 74- 88 GHz, respectively. The measured average power gain is 10.1-18.9 dB at 76-84 GHz with the rms gain error of < 0.6 dB at 76-77 GHz, < 0.8 dB at 79-81 GHz and < 1.1 dB at 81- 84 GHz. The measured rms phase error is < 3.9° at 76-77 GHz, < 7.2° at 79-81 GHz and < 10.4° at 81-84 GHz. The measured NF is 10.5 +/- 0.5 dB at 80 GHz and the measured input P1dB is -26.7 dBm to -23 dBm at 77-80 GHz depending on the gain setting. The on-chip coupling is < -30 dB between adjacent channels. Finally, a 76-84 GHz 16-element phased array receiver in a 0.13 [mu]m SiGe BiCMOS process is presented. All circuits are designed differentially to result in less sensitivity to packaging effect and high channel-to-channel isolation. The overall chip size is 5.0 x 5.8 mm� with the power consumption of 500-600 mA from 2 V supply voltage. The measured Sv(1)1 and Sv(2)2 for all 16 phase states is < -9 dB at 72-88 GHz and 73-86 GHz, respectively. And the measured average power gain (Sv(2)v(1)) is > 10 dB for 76.4-90 GHz with the rms gain error of < 1 dB for 74-84.2 GHz. The measured rms phase error is < 11� for 73.6-83.6 GHz. In order to optimize the rms gain and phase errors, the VGA and 11� phase shifter are used. The measured reverse isolation (Sv(1)v(2)) is > -45 dB. The measured NF is 11.2-13 dB at 77-87 GHz at the maximum gain state. And the measured input P1dB is -20 dBm at 77 GHz and -25.8 dBm at the 83 GHz. The measured coupling between channels is < -48 dB because of the relatively high substrate resistance and the long distance between channels
    Cover page: W-band phased array systems using silicon integrated circuits
    • Article
    • Peer Reviewed
    UC Riverside Previously Published Works (2019)
    Macrophages are critically involved in wound healing, from dampening inflammation to clearing cell debris and coordinating tissue repair. Within the wound, the complexity of macrophage function is increasingly recognized, with adverse outcomes when macrophages are inappropriately activated, such as in fibrosis or chronic non-healing wounds. Recent advances in in vivo and translational wound models, macrophage-specific deletions and new technologies to distinguish macrophage subsets, have uncovered the vast spectrum of macrophage activation and effector functions. Here, we summarize the main players in wound-healing macrophage activation and function, including cytokines, apoptotic cells, nucleotides and mechanical stimuli. We highlight recent studies demonstrating cooperation between these factors for optimal wound healing. Next, we describe recent technologies such as cell tracking and single-cell RNA-seq, which have uncovered remarkable plasticity and heterogeneity in blood-derived or tissue-resident macrophages and discuss the implications for wound healing. Lastly, we evaluate macrophage dysfunction in aberrant wound healing that occurs in aging, diabetes and fibrosis. A better understanding of the longevity and plasticity of wound-healing macrophages, and identification of unique macrophage subsets or specific effector molecules in wound healing, would shed light on the therapeutic potential of manipulating macrophage function for optimal wound healing.
      Cover page: Macrophages in wound healing: activation and plasticity.
      • Thesis
      • Peer Reviewed
      UC Berkeley Electronic Theses and Dissertations (2011)

      This dissertation details the synthesis and properties of Ca-doped BiFeO3 thin films. The phase diagram was established as a function of the Ca doping concentration and temperature through structural analysis to study the effect of divalent-ion-calcium doping on BiFeO3 films. A ferroelectric-paraelectric boundary exists around at 10% Ca doping ratio. For this doping concentration, the largest transition of conduction states was observed. The mechanisms for the observed effects are discussed on the basis of the interplay of ionic and electronic conduction through the redistribution of oxygen vacancies by application of electric fields. Application of electric fields enables to control and manipulate this electronic transition to the extent that a p-n junction can be created, erased and inverted in this material. Beside this conduction transition, the visible shading effect was observed with application of electric fields. Based on these reversible transitions of the electrical and optical characteristics of Ca-doped BiFeO3, electrical and optical memory devices are proposed in this dissertation. The memory device built with a hetero-junction presented a nonvolatile conduction modulation with a rectified current behavior, which is essential for realizing random access memory devices. The switching mechanism is elucidated by junction property modification ascribed to the change of local oxygen vacancy concentration. In addition, the optical characteristics of Ca-doped BiFeO3 films for potential electro-optic memory devices were measured and evaluated. Detailed discussion about the origin of the shading effect is given based on the change of a polar order parameter and an oxygen vacancy ordered state.

        Cover page: Electric Modulation of Conduction and Optical Characteristics in Ca-doped BiFeO3 Films for Memory Device Applications
        • Multimedia
        CMPM 80K (2019)
        The main gameplay goal is a game with high replayability and simple controls, somewhat similar to the classic arcade games. This game has similar classic air combat games. That is, the player has to evade every bullet (for this case, every teacup) and survive as much as you can. With several innovative difference, which will be described in a later paragraph, this is a typical arcade game, so high replay-ability of replay is quite achieved in considerable degree. And there are only two kinds of keys, which are using items and moving horizontally. And there can be only 3 positions that players can place. So simple control is also achieved.The main aesthetic goal is to achieve strong cohesion between theme and gameplay. Our theme is ‘Alice in the Wonderland’, more specifically the falling scene when Alice enters the rabbit hole. This falling theme is not only closely related to the gameplay mechanics but also the theme word we provided from the lecture. Artworks are carefully chosen to represent the ‘Alice in the wonderland’ theme. Rabbit’s clock, the ‘Drinkme’ potion, Ace of Heart and the teacups are all directly related to the important imageries of the story. Even the game music, which is not composed by ourselves, is sharing the same theme of us. Except for Alice’s explosion at the end, all of the details are closely linked to the theme. So we think our aesthetic goal is achieved.As we learned from the lecture, the decision is what makes a game interesting. If there are too many decisions to make at one time, it makes players confused. But if there are too few options for the decision, it will make a game boring. At first sight, it seems that our game is a simple no-brainer dexterity game. That is not true. The Ace of Heart cards, which can eliminate upcoming teacups, are the most common items in the game. You can use this item right away, or keep it till the stage becomes much harder. This makes the players make a choice and strategy. Also, there is another kind of decision there. If players collide to the rabbit’s clock, it will grant 50 points, which is five times of normal teacup breaking points. However, the rabbit’s clock reverses the direction of teacup for 2 seconds and reverse again. During this time, the movement pattern of teacups is confusing. So it is likely to kill player because of it. A player can choose between to raise a score by going through a risky way or to choose a safe way by giving extra points away. This choice happens periodically. This is why this game is really addictive. I guess this is also related to the operant conditioning, which was covered in the lecture.We tried to design a fresh game with some innovative features. Actually, we are not deep into the air combat game, which is perhaps the most similar kind of game to ours. Our ignorance liberated us from the genre’s cliche and encouraged us to make peculiar features. For example, there is no enemy to fight against here. Instead of making an enemy to conquer, we just throw players in infinite teacup rain. Furthermore, we give users a limited power for active shooting. This decision is mainly due to the theme we implemented and the limitation of a number of total events. And we don’t think that kind of enemy is really necessary here. Big differences to relatives but a satisfying one. The time-traveling rabbit’s clock and 'Drinkme' potion, which temporarily reduces the size of Alice, is also unique items in this game. One of the most important innovations in our game is a strongly convincing theme of items. In combat games, items look like military supplies which are quite general and boring. In our game, we used game items from the original story so that we can understand what will happen if we use those items even before we really play it. We reflected several feedbacks from playtesters in our final beta version. One of the most important change is the UI. Before the beta version, we try to explain every important rule using plain texts. But after we got the feedback, we realize an image base description will improve UI and the player’s understanding of the game. Some feedbacks are really critical to the gameplay. Every velocity in the game, including falling of Alice, speed of cups and items, and even speed of background is half as slow when we first built the alpha version. This version can easily lose tension and even harder for it has non-intuitive timing. This problem was also discussed feedback so we fixed it.'
        • 1 supplemental ZIP
        Creative Commons 'BY-NC' version 4.0 license
        • Thesis
        • Peer Reviewed
        UC Irvine Electronic Theses and Dissertations (2014)

        This study explains how new science-based knowledge is adopted by diverse organizations, which over time creates the conditions for emergence of a new organizational community. I focus on the role of technological systems in emergence of a science-based community. A technological system is defined as regional sources of knowledge and competence that develop and diffuse technical and scientific knowledge in emerging fields of science. I argue that technological systems enhance the visibility of new science and novel technology, promote resource spillovers, assist identity construction, and attract entrepreneurs to apply the new technology to new business opportunities. As a result, many organizations originating in separate existing communities increasingly become involved in developing and commercializing a new technology, which over time, creates the nucleus for new community emergence.

        Focusing on emergence of a nanotechnology community in the U.S. between 1959 and 2004, I investigate that technological systems can emerge through scientific collaboration; size of technological systems can foster emergence of de novo organizations dedicated to the new knowledge; and technological systems can reinforce the knowledge flow between universities and industries to facilitate emergence of a new community.

        First, I contend that scientific collaboration, defined as co-authorship based on new scientific knowledge, can lead to the emergence of technological-system formation. Specifically, it is found that intensity and heterogeneity of scientific collaboration speeds up the formation of technological systems. Second, the role of technological systems in community creation is discussed, arguing that size of technological systems, specified into depth (i.e. the number of components) and breadth (i.e. the number of subsystems), has impacts on community creation. The estimation results show that both depth and breadth increase the likelihood of de novo foundings and population differentiation. Last, knowledge flow between universities and industries is specified into knowledge streaking (collaboration ties) and knowledge leaking (citation ties). The estimation results reveal that knowledge streaking and inflow of knowledge leaking are positively related to the founding rate of new firms and the rate of population differentiation. Also, the relation between the inflow of knowledge leaking and community creation is reinforced by research centers.

          Cover page: The Role of Technological Systems in Community Creation: Emergence of a Nanotechnology Community, 1959-2004
          • Article
          • Peer Reviewed
          UC Riverside Previously Published Works (2019)
          Macrophages are critically involved in wound healing, from dampening inflammation to clearing cell debris and coordinating tissue repair. Within the wound, the complexity of macrophage function is increasingly recognized, with adverse outcomes when macrophages are inappropriately activated, such as in fibrosis or chronic non-healing wounds. Recent advances in in vivo and translational wound models, macrophage-specific deletions and new technologies to distinguish macrophage subsets, have uncovered the vast spectrum of macrophage activation and effector functions. Here, we summarize the main players in wound-healing macrophage activation and function, including cytokines, apoptotic cells, nucleotides and mechanical stimuli. We highlight recent studies demonstrating cooperation between these factors for optimal wound healing. Next, we describe recent technologies such as cell tracking and single-cell RNA-seq, which have uncovered remarkable plasticity and heterogeneity in blood-derived or tissue-resident macrophages and discuss the implications for wound healing. Lastly, we evaluate macrophage dysfunction in aberrant wound healing that occurs in aging, diabetes and fibrosis. A better understanding of the longevity and plasticity of wound-healing macrophages, and identification of unique macrophage subsets or specific effector molecules in wound healing, would shed light on the therapeutic potential of manipulating macrophage function for optimal wound healing.
            Cover page: Macrophages in wound healing: activation and plasticity
            • Article
            • Peer Reviewed
            UC San Francisco Previously Published Works (2018)
            Previous work by Kim, et al. (2017) unveiled that lysyl-tRNA synthetase (KRS) is secreted through a mechanism involving syntenin-containing exosomes. They described how KRS, commonly known as part of the translational machinery in the cytoplasm, is secreted into the extracellular space where it induces inflammation. First, KRS secretion is triggered by starvation conditions. The increase in caspase-8 levels during starvation is responsible for proteolysis and generation of the N-terminal truncated form of KRS, and this event is required for KRS dissociation from the multi-synthetase complex (MSC). N-terminal cleavage of KRS eventually leads to a conformational change that allows its interaction with the C-terminal PDZ binding motif of syntenin and subsequent exosome biogenesis. The KRS-syntenin complex translocates to multivesicular bodies (MVBs) that originate from endosomes involved with intraluminal vesicle (ILVs). MVBs are transporters for the secretion of cellular contents into the extracellular space. Syntenin localizes intraluminal vesicles within endosomal membranes. The KRS-syntenin complex transfers on to intraluminal vesicles in MVBs. MVBs are translocated to the plasma membrane for ILV secretion mediated by Rab family proteins. Once KRS exosomes are secreted, their membranes are eventually ruptured by proteases and KRS is released from the exosomes where it can act as an inflammatory cytokine in the extracellular space. Secreted KRS triggers macrophage/neutrophil migration and induces inflammation.
              Cover page: Exosomal secretion of truncated cytosolic lysyl-tRNA synthetase induces inflammation during cell starvation
              • Thesis
              • Peer Reviewed
              UC Riverside Electronic Theses and Dissertations (2022)

              Preclinical models of infection, such as murine infection models and transgenic mice, provide critical knowledge for the treatment and diagnosis of infections of significant public health concern. In particular, the mucosal barrier, such as the lung and intestine are susceptible to multiple infectious pathogens given their exposure to the external environment. The goal of this dissertation was to investigate the function of RELMα and CX3CR1 in mucosal infections with parasitic helminths and influenza virus, as these are pathogens of significant health concern worldwide. RELMα is a mouse protein, which has orthologs in humans such as resistin and RELMβ. First, we tested the function of RELMα and investigated factors that may regulate its expression in infection. RELMα accelerated resolution of inflammation and tissue repair in infection with mouse intestinal helminth Heligmosomoides polygyrus. We also discovered that choline kinase signaling was critical for optimal RELMα expression: when mice were infected with H. polygyrus and injected with choline kinase alpha inhibitor, RSM-932A, alternative activation of macrophages and RELMα expression was downregulated in RSM-932A-injected mice. Previous studies have reported RELMα expression in type 2 cytokine inflammation, however, the functional relevance of RELMα in other infectious contexts, such as viral infections, is unclear. RELMα was induced by IAV infection in the BALF and airway epithelial cells. RELMα induced influenza infections in mouse lung epithelial cells in vitro and in vivo, suggesting that RELMα expressed in lung epithelial cells promotes influenza infection of neighboring cells. In the last chapter of this thesis, we broadened our research scope to investigate the function of myeloid-derived cells in helminth infection by targeting CX3CR1, a critical chemokine receptor for monocyte recruitment from the blood vessel to the site of infection. CX3CR1 deficiency induced a more inflammatory response but lower parasite burden in the lung. CX3CR1-deficient monocytes were more cytotoxic and active than WT monocytes, demonstrating the regulatory function of CX3CR1 in monocytes. Collectively, these studies demonstrate diverse functions of RELMα and CX3CR1 in different infectious diseases and identify putative downstream targets by which RELMα and CX3CR1 modulate the immune response and tissue repair.

              • 1 supplemental PDF
              Cover page: Innate Immune Responses to Mucosal Infection are Regulated by RELMα
              • Article
              • Peer Reviewed
              Research Grants Program Office (RGPO) Funded Publications (2012)
              Secondhand smoke (SHS) exposure is a known risk factor for lung cancer development in lifelong nonsmokers; however, the mechanistic involvement of SHS in the genesis of this malignancy remains elusive. The present study is the first comprehensive investigation of SHS mutagenicity in vivo, in which we have established the mutagenic effects of SHS in transgenic Big Blue mice, and subsequently found correlations between our experimental findings and those obtained from our analysis of the largest database of mutations in human TP53, which is the most frequently mutated gene in human lung cancer. We demonstrate that whole-body SHS exposure of mice for 5 h/d, 5 d/wk for a duration of 2 or 4 mo elicits a significant mutagenic response in the lung, trachea, and bladder of exposed animals, as reflected by the elevation of background cII mutant frequency in the respective organs. The organ-specific mutagenicity of SHS is most pronounced in the lung and remains persistent both in the lung and bladder of SHS-exposed animals after a 1-mo recovery in clean air. The induced cII mutagenesis in the lung of SHS-exposed mice perfectly recapitulates our analysis of the TP53 mutations in human lung cancer in nonsmokers. Remarkably, the relative frequencies of all types of mutations in the TP53 gene of nonsmokers' lung tumors and in the cII transgene of lung cellular DNA from SHS-exposed mice are indistinguishable from one another. We provide the first verification of a mechanistic mode of action for SHS of relevance for carcinogenesis and the first experimental evidence linking SHS exposure to lung cancer in nonsmokers.
                Cover page: New experimental data linking secondhand smoke exposure to lung cancer in nonsmokers
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