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Open Access Publications from the University of California

Scholarly Works (715 results)

  • Article
  • Peer Reviewed
UCLA Previously Published Works (2024)
Urinary symptoms are one of the most common reasons for emergency visits in females of pediatric age group and can be associated with various conditions like infections (most common), sexual trauma and rarely neoplastic processes. Here, we report a case of a 7-year-old female who presented in the emergency multiple times with the complaints of urinary symptoms and vaginal pain and was empirically treated with antibiotics and antifungals without symptomatic improvement. Her blood tests, physical examination during this time remained unrevealing. She was then transferred to our institution on her third emergency visit for further evaluation. On imaging studies, she was noted to have expansile lesions on her vertebral body at the L4 and T6 levels with compressive myelopathy with multiple bone and soft tissue lesions throughout her lower extremities. Patient developed saddle anesthesia requiring emergent decompression and biopsy of the epidural mass with the final pathology coming back as B-lymphoblastic leukemia/lymphoma. B-ALL/B-LBL is the most common pediatric hematologic malignancy and usually presents with fever, hepatosplenomegaly, lymphadenopathy, bone pain and bleeding. Occasionally, atypical presentations like bone and joint pain, osteoporosis, palpable paravertebral mass have been described. However, this is the first case report to describe a very unusual and unfamiliar presentation of this disease causing significant diagnostic difficulty resulting in delayed treatment. This case report can aid as a reminder that unusual pain or any nonspecific manifestations in pediatric patients, refractory to common treatment should be investigated with extreme diligence not to miss this neoplastic process.
    Cover page: Dysuria and Vaginal Pain, Unusual Manifestations of B-acute Lymphoblastic Lymphoma.
    • Thesis
    • Peer Reviewed
    UC San Diego Electronic Theses and Dissertations (2012)
    The dissertation comprises two separate topics. Chapters 2 and 3 are experimental studies on remanence acquisition processes. Chapters 4 and 5 investigate the geomagnetic field variability in Africa and India between 1000 BCE and 1000 CE. Chapter 2 is a study in which the role of flocculation in sedimentary magnetization is analyzed with the help of laboratory redeposition experiments and a simple numerical model. At small floc sizes DRM acquisition is likely to be non-linear but it may record the directions with higher fidelity. In environments having bigger flocs the sediments are likely to record either intensities or directions with high fidelity, but not both. Also flocculation may inhibit a large fraction of magnetic grains from contributing to the net remanence and this might have consequences for intensity normalization in sediments. Chapter 3 presents a fresh perspective on the long standing debate of the nature of magnetocrystalline anisotropy in Mid-Ocean Ridge Basalts (MORBs). A new parameter, IRAT, defined as the ratio of the isothermal remanences in antiparallel directions is used to differentiate between uniaxial single domain grains (IRAT ̃1) and multiaxial single domain grains (IRAT <1). The theoretical predictions were first validated with standard samples and then multiple MORB samples were analyzed. The observed IRAT ratios indicate a dominant non -uniaxial anisotropy in the MORBs. Chapters 4 and 5 are archeointensity studies from two data poor regions of the world viz., Africa and India. With stringent data selection criteria and well established archeological constraints these datasets provide important constraints on the field intensity from 1000 BCE to 1000 CE in Africa and 500 BCE to 1000 CE in India. The African dataset has a higher age resolution than the Indian dataset. The African dataset matches well with the global CALS3k.4 model and shows significant non-axial-dipolar contribution in the region. The Indian dataset is not of a similar resolution but shows that the field might have dropped by as much as 40% in the first half of the first century BCE and remained low during the first century CE
      Cover page: Experimental studies on remanence acquisition processes and regional geomagnetic field variability from archeointensity studies
      • Article
      • Peer Reviewed
      UC Davis Previously Published Works (2016)

      Aim

      To quantify the progression and severity of mouse collagen-induced arthritis (CIA) using an in vivo imaging tool, (18) F-fluorodeoxyglucose ((18) F-FDG) PET/CT and validate it against gold standard 'histopathological' evaluation.

      Method

      The PET radiotracer (18) F-FDG, a marker for glucose metabolism, was injected in mice at different stages of CIA and the radiotracer distribution was imaged using a PET scanner. A sequential CT scan provided correlated anatomy. Radiotracer concentration was derived from PET/CT images for individual limb joints and on a per-limb basis at different stages of the disease. The imaging outcomes were subjected to correlation analysis with concurrently measured clinical and histological score.

      Results

      Clinical and histological score, and hence disease severity, showed a strong linear correlation (r(2)  = 0.71, P = 0.001 and r(2)  = 0.87, P < 0.001, respectively) with radiotracer concentration measured from PET/CT during the progression of CIA.

      Conclusions

      The strong positive correlation of the (18) F-FDG PET/CT findings with the histopathological evaluation at different stages of the disease suggest the potential of this imaging tool for the non-invasive assessment of progression and severity in mouse autoimmune arthritis. Thus, in preclinical studies, (18) F-FDG PET/CT can be considered as a non-invasive tool to develop novel therapies of inflammatory arthritis.
        Cover page: In vivo quantification of mouse autoimmune arthritis by PET/CT
        • Article
        • Peer Reviewed
        Proceedings of the Annual Meeting of the Cognitive Science Society, Volume 44 (2022)
        A previous study used the Antarjami gaming framework to determine the OCEAN personality traits. In this study, a reinforcement learning agent is being compared to its human counterpart through various levels in the game. A Deep-Q Network(DQN) is proposed here for playing the Antarjami game autonomously. The DQN takes as input the image of the game screen and decides the moves/actions it wants to play in the game. A collection of DQNs having uniform architectures is used, where each DQN is trained on a particular level of the game. The starting position of each player within a game level is random in the Antarjami framework, therefore the training of the reinforcement learning agent is agnostic to any bias about the initial positions of the players. The work shows how an RL-Agent gathers scores in a greedy fashion irrespective of any psychological inclinations.
          Cover page: A Study on Relative Performance of an Reinforcement Learning Agent and Human in a Psychometric Assessment GameCreative Commons 'BY' version 4.0 license
          • Article
          • Peer Reviewed
          UC Davis Previously Published Works (2022)
          The global pandemic of coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has shaken the entire world. The social, health and financial impacts of this pandemic are beyond words. We have learnt a lot about this new disease in a short period of time, but still a long road to go to fully determine its pathogenic effect. The primary target of this virus is angiotensin-converting enzyme 2 (ACE2) receptor, which is prevalent in endothelial cells throughout the body. Immunocompromised patients such as patients with sickle cell disease are more vulnerable to severe respiratory infections, including infection with SARS-CoV-2. In addition, sickle cell disease patients are prone to vaso-occlusive crisis, and theoretically SARS-CoV-2 can worsen the situation as it also can cause endothelial dysfunction and thrombosis. Herein, we are sharing an interesting peripheral blood smear finding of an asymptomatic 31-year-old multigravida pregnant female with a history of sickle cell disease and found to have a positive COVID-19 polymerase chain reaction (PCR) test during her third trimester of pregnancy at a routine clinic visit. Two weeks after the initial positive test, she developed nausea, vomiting, constipation and a pain crisis affecting her extremities while her COVID-19 PCR test was still positive. She was hemodynamically stable, and lab workup revealed chronic anemia, leukocytosis with neutrophilia and lymphopenia. Morphologic examination of the peripheral blood smear showed a marked leukoerythroblastosis: rare myeloblasts, sickle cells, markedly abundant nucleated red blood cells (RBCs), metamyelocytes, and many large and giant platelets were seen. In this context, her previous peripheral blood smears (prior to positive COVID-19 test) did not show leukoerythroblastosis. She was managed conservatively with hydration and pain control and delivered at 36 weeks via cesarean section due to pre-term labor and intrauterine growth retardation. The unusual finding of leukoerythroblastosis in a pregnant sickle cell disease patient with an asymptomatic COVID-19 infection indicates further studies to determine its effect on hematopoietic system and elucidate its clinical significance.
            Cover page: Leukoerythroblastosis in a Sickle Cell Patient With Pregnancy: An Interesting Peripheral Blood Smear Finding.
            • Article
            • Peer Reviewed
            UC Davis Previously Published Works (2024)
            COVID-19 infection is still a mystery in terms of its long-term effect on health and its consequences on hematological disorders. Prior studies including ours have shown the abnormal changes in hematopoietic cells in COVID-19 patients. In this article, we are presenting 2 cases of pediatric B-lymphoblastic leukemia (B-ALL) with a previous history of COVID-19 infection. The first case describes a 22-month-old boy presenting with lymphadenopathy, neutropenia, and anemia with concurrent COVID-19 infection without any evidence of a hematolymphoid neoplasm as per bone marrow and lymph node biopsy. However, he presented after 2 months with bone marrow biopsy confirming B-ALL. The second case is that of a 4-year-old girl presenting with B-ALL who has had asymptomatic COVID-19 infection 5 months before this current presentation. Both the cases had complete resolution of COVID-19 infection during the time of presentation with acute leukemia. There were notably 2 rare findings along the course of the patients illnesses. First, the unusual plasmacytosis in the marrow during active COVID-19 infection in the first patient and the second, is predilection of development of B-ALL following COVID-19. In both the cases the fluorescence in situ hybridization (FISH) studies showed pathologic alteration of the RUNX1 gene. Overall, there are no literature to support a causal association between acute B-ALL and COVID-19. The diagnosis of B-ALL in these patients after COVID-19 infection may be totally unrelated. However, if we consider Greaves proposed 2-hit model for childhood acute leukemia, that an infectious agent can precipitate development of B-ALL in a genetically susceptible individual. Alteration of the RUNX1 gene in both the patients, opens a door for further exploration of the second-hit hypothesis regarding an infectious agent precipitating development of B-ALL in a genetically susceptible individual.
              Cover page: Diagnosing B-cell acute lymphoblastic leukemia in 2 pediatric patients with recent SARS-CoV-2 infection.
              • Article
              • Peer Reviewed
              UC San Francisco Previously Published Works (2008)
              The accumulation of mutant protein is a common feature of neurodegenerative disease. In Huntington's disease, a polyglutamine expansion in the huntingtin protein triggers neuronal toxicity. Accompanying neuronal death, mutant huntingtin aggregates in large macromolecular structures called inclusion bodies. The function of the machinery for intracellular protein degradation is linked to huntingtin toxicity and components of this machinery colocalize with inclusion bodies. An increasing body of evidence implicates the ubiquitin-proteasome pathway in the failure of cells to degrade mutant huntingtin. A number of potential mechanisms that link compromised ubiquitin-proteasome pathway function and neurodegeneration have been proposed and may offer opportunities for therapeutic intervention.
                Cover page: The Ubiquitin-Proteasome Pathway in Huntington's Disease
                • Thesis
                • Peer Reviewed
                UC Riverside Electronic Theses and Dissertations (2021)

                This thesis contains research conducted on various topics in quantum Hall physics and deep learning theory. The first chapter studies a particular aspect of quantum Hall systems, namely their behavior around the $\nu = 1/2$ Landau level (LL) state. This work is motivated by the need to understand better this particular state in light of the two proposed distinct theoretical descriptions existing for the same. Specifically, we analyze quantum oscillations around the $\nu = 1/2$ LL state using one of the propositions to support the latter. The second and third chapters study two distinct domains in deep learning, multi and single-objective models. In particular, the second considers a specific type of multi-objective model, zero-sum games, to demonstrate existing issues in training such setups and develop an efficient optimization scheme. The final chapter involves studying a particular aspect of the generalization behavior of deep neural networks (DNNs). Specifically, it attempts to provide a theoretical framework to explain the recently observed phenomenon of "epoch-wise double descent" in such DNNs.

                  Cover page: Topics in Quantum-Hall Physics, Game-Optimization and Generalization in Neural Networks
                  • Thesis
                  • Peer Reviewed
                  UC San Francisco Electronic Theses and Dissertations (2007)

                  Huntington's disease is a devastating inherited neurodegenerative disorder without a cure. Mutations expanding a stretch of glutamines in the first exon of the widely-expressed huntingtin protein are responsible for Huntington's disease. The disease is characterized by neuronal death within the striatum and cortex. At the cellular level, abnormal inclusions of ubiquitinated huntingtin are present in affected brain areas. The role of inclusions in cellular pathogenesis has been controversial, with inclusions potentially playing protective, detrimental, or incidental roles. We developed a high-throughput robotic imaging and analysis platform that enables us to follow the fates of individual cells and intracellular proteins over time. This platform represents a significant improvement over standard approaches of cell-population based biochemistry and conventional time-lapse microscopy in being able to monitor molecular changes as they unfold in large numbers of live cells and in quantifying the extent to which these changes predict cellular outcomes. Using this platform, we followed individual neurons expressing mutant huntingtin and determined that cells that form inclusions survive better than those that do not. Levels of mutant protein were higher in those cells that formed inclusions and in those cells that died earlier. Through the use of fluorescent reporters of ubiquitin-proteasome system function, we determined that impairment of the ubiquitin-proteasome system is toxic to neurons and is higher in cells that go on to form inclusions compared to those that do not. Following inclusion formation, ubiquitin-proteasome system function is improved. Our data unambiguously shows that inclusions are beneficial to neuronal survival and that part of this beneficial effect may be through improving ubiquitin-proteasome system function. These findings shift the focus to steps preceding inclusion formation in the search for the molecular species responsible for Huntington's disease.

                    Cover page: Understanding the cellular pathogenesis of Huntington's disease
                    • Article
                    Posters (2006)

                    Optimal power allocation, in a wireless sensor network with a fusion center, for distributed parameter estimation under a total network power constraint is considered. For the simple star topology, an analysis of the effect of the measurement noise variance on the optimal power allocation policy is presented. As the measurement noise variance increases, the optimal solution evolves from sensor selection to power equalization - the sensor with the lowest SNR is allocated the largest fraction of the total power.Relaying nodes are introduced to form more complicated branch, tree and linear topologies. The optimal power allocation strategies for these topologies are then considered for both amplify-and-forward and estimate-and-forward transmission protocols. Analytical solutions for these cases are intractable, and thus asymptotically (for increasing measurement noise variance) optimal solutions are derived.

                      Cover page: Optimal Power Allocation in Distributed Sensing (SEN 3)
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