Browsing by Author "Wang, Jing"
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Item Assessing Progress Toward the Vision of a Comprehensive, Shared Electronic Care Plan: Scoping Review(JMIR, 2022-06-10) Norton, Jenna M.; Ip, Alex; Ruggiano, Nicole; Abidogun, Tolulope; Camara, Djibril Souleymane; Fu, Helen; Hose, Bat-Zion; Miran, Saadia; Hsiao, Chun-Ju; Wang, Jing; Bierman, Arlene S.; Epidemiology, Richard M. Fairbanks School of Public HealthBackground: Care plans are central to effective care delivery for people with multiple chronic conditions. But existing care plans-which typically are difficult to share across care settings and care team members-poorly serve people with multiple chronic conditions, who often receive care from numerous clinicians in multiple care settings. Comprehensive, shared electronic care (e-care) plans are dynamic electronic tools that facilitate care coordination and address the totality of health and social needs across care contexts. They have emerged as a potential way to improve care for individuals with multiple chronic conditions. Objective: To review the landscape of e-care plans and care plan-related initiatives that could allow the creation of a comprehensive, shared e-care plan and inform a joint initiative by the National Institutes of Health and the Agency for Healthcare Research and Quality to develop e-care planning tools for people with multiple chronic conditions. Methods: We conducted a scoping review, searching literature from 2015 to June 2020 using Scopus, Clinical Key, and PubMed; we also searched the gray literature. To identify initiatives potentially missing from this search, we interviewed expert informants. Relevant data were then identified and extracted in a structured format for data synthesis and analysis using an expanded typology of care plans adapted to our study context. The extracted data included (1) the perspective of the initiatives; (2) their scope, (3) network, and (4) context; (5) their use of open syntax standards; and (6) their use of open semantic standards. Results: We identified 7 projects for e-care plans and 3 projects for health care data standards. Each project provided critical infrastructure that could be leveraged to promote the vision of a comprehensive, shared e-care plan. All the e-care plan projects supported both broad goals and specific behaviors; 1 project supported a network of professionals across clinical, community, and home-based networks; 4 projects included social determinants of health. Most projects specified an open syntax standard, but only 3 specified open semantic standards. Conclusions: A comprehensive, shared, interoperable e-care plan has the potential to greatly improve the coordination of care for individuals with multiple chronic conditions across multiple care settings. The need for such a plan is heightened in the wake of the ongoing COVID-19 pandemic. While none of the existing care plan projects meet all the criteria for an optimal e-care plan, they all provide critical infrastructure that can be leveraged as we advance toward the vision of a comprehensive, shared e-care plan. However, critical gaps must be addressed in order to achieve this vision.Item Displacement of WDR5 from Chromatin by a WIN Site Inhibitor with Picomolar Affinity(Elsevier, 2019-03-12) Aho, Erin R.; Wang, Jing; Gogliotti, Rocco D.; Howard, Gregory C.; Phan, Jason; Acharya, Pankaj; Macdonald, Jonathan D.; Cheng, Ken; Lorey, Shelly L.; Lu, Bin; Wenzel, Sabine; Foshage, Audra M.; Alvarado, Joseph; Wang, Feng; Shaw, J. Grace; Zhao, Bin; Weissmiller, April M.; Thomas, Lance R.; Vakoc, Christopher R.; Hall, Matthew D.; Hiebert, Scott W.; Liu, Qi; Stauffer, Shaun R.; Fesik, Stephen W.; Tansey, William P.; Biochemistry and Molecular Biology, School of MedicineThe chromatin-associated protein WDR5 is a promising target for pharmacological inhibition in cancer. Drug discovery efforts center on the blockade of the "WIN site" of WDR5, a well-defined pocket that is amenable to small molecule inhibition. Various cancer contexts have been proposed to be targets for WIN site inhibitors, but a lack of understanding of WDR5 target genes and of the primary effects of WIN site inhibitors hampers their utility. Here, by the discovery of potent WIN site inhibitors, we demonstrate that the WIN site links WDR5 to chromatin at a small cohort of loci, including a specific subset of ribosome protein genes. WIN site inhibitors rapidly displace WDR5 from chromatin and decrease the expression of associated genes, causing translational inhibition, nucleolar stress, and p53 induction. Our studies define a mode by which WDR5 engages chromatin and forecast that WIN site blockade could have utility against multiple cancer types.Item Emerging Landscape of Preclinical Models for Studying COVID-19 Neurologic Diseases(American Chemical Society, 2023-09-06) Li, Jason; Wang, Jing; Wang, Hu; Neurology, School of MedicineCOVID-19 (Coronavirus Disease 2019) is an infectious disease caused by SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2) and has globally infected 768 million people and caused over 6 million deaths. COVID-19 primarily affects the respiratory system but increasing reports of neurologic symptoms associated with COVID-19 have been reported in the literature. The exact mechanism behind COVID-19 neurologic pathophysiology remains poorly understood due to difficulty quantifying clinical neurologic symptoms in humans and correlating them to findings in human post-mortem samples and animal models. Thus, robust preclinical experimental models for COVID-19 neurologic manifestations are urgently needed. Here, we review recent advances in in vitro, in vivo, and other models and technologies for studying COVID-19 including primary cell cultures, pluripotent stem cell-derived neurons and organoids, rodents, nonhuman primates, 3D bioprinting, artificial intelligence, and multiomics. We specifically focus our discussion on the contribution, recent advancements, and limitations these preclinical models have on furthering our understanding of COVID-19's neuropathic physiology. We also discuss these models' roles in the screening and development of therapeutics, vaccines, antiviral drugs, and herbal medicine, and on future opportunities for COVID-19 neurologic research and clinical management.Item Health information technology to improve care for people with multiple chronic conditions(Wiley, 2021) Samal, Lipika; Fu, Helen N.; Camara, Djibril S.; Wang, Jing; Bierman, Arlene S.; Dorr, David A.; Epidemiology, Richard M. Fairbanks School of Public HealthObjective: To review evidence regarding the use of Health Information Technology (health IT) interventions aimed at improving care for people living with multiple chronic conditions (PLWMCC) in order to identify critical knowledge gaps. Data sources: We searched MEDLINE, CINAHL, PsycINFO, EMBASE, Compendex, and IEEE Xplore databases for studies published in English between 2010 and 2020. Study design: We identified studies of health IT interventions for PLWMCC across three domains as follows: self-management support, care coordination, and algorithms to support clinical decision making. Data collection/extraction methods: Structured search queries were created and validated. Abstracts were reviewed iteratively to refine inclusion and exclusion criteria. The search was supplemented by manually searching the bibliographic sections of the included studies. The search included a forward citation search of studies nested within a clinical trial to identify the clinical trial protocol and published clinical trial results. Data were extracted independently by two reviewers. Principal findings: The search yielded 1907 articles; 44 were included. Nine randomized controlled trials (RCTs) and 35 other studies including quasi-experimental, usability, feasibility, qualitative studies, or development/validation studies of analytic models were included. Five RCTs had positive results, and the remaining four RCTs showed that the interventions had no effect. The studies address individual patient engagement and assess patient-centered outcomes such as quality of life. Few RCTs assess outcomes such as disability and none assess mortality. Conclusions: Despite a growing body of literature on health IT interventions or multicomponent interventions including a health IT component for chronic disease management, current evidence for applying health IT solutions to improve care for PLWMCC is limited. The body of literature included in this review provides critical information on the state of the science as well as the many gaps that need to be filled for digital health to fulfill its promise in supporting care delivery that meets the needs of PLWMCC.Item Heat shock protein 90 promotes RNA helicase DDX5 accumulation and exacerbates hepatocellular carcinoma by inhibiting autophagy(China Anti-Cancer Association, 2021-03-25) Zhang, Ting; Yang, Xinrui; Xu, Wanping; Wang, Jing; Wu, Dawei; Hong, Zhixian; Yuan, Shengxian; Zeng, Zhen; Jia, Xiaodong; Lu, Shanshan; Safadi, Rifaat; Han, Sen; Yang, Zhihong; Neckers, Leonard M.; Liangpunsakul, Suthat; Zhou, Weiping; Lu, Yinying; Medicine, School of MedicineObjective: Hepatocellular carcinoma (HCC), the main type of liver cancer, has a high morbidity and mortality, and a poor prognosis. RNA helicase DDX5, which acts as a transcriptional co-regulator, is overexpressed in most malignant tumors and promotes cancer cell growth. Heat shock protein 90 (HSP90) is an important molecular chaperone in the conformational maturation and stabilization of numerous proteins involved in cell growth or survival. Methods: DDX5 mRNA and protein expression in surgically resected HCC tissues from 24 Asian patients were detected by quantitative real-time PCR and Western blot, respectively. The interaction of DDX5-HSP90 was determined by molecular docking, immunoprecipitation, and laser scanning confocal microscopy. The autophagy signal was detected by Western blot. The cell functions and signaling pathways of DDX5 were determined in 2 HCC cell lines. Two different murine HCC xenograft models were used to determine the function of DDX5 and the therapeutic effect of an HSP90 inhibitor. Results: HSP90 interacted directly with DDX5 and inhibited DDX5 protein degradation in the AMPK/ULK1-regulated autophagy pathway. The subsequent accumulation of DDX5 protein induced the malignant phenotype of HCC by activating the β-catenin signaling pathway. The silencing of DDX5 or treatment with HSP90 inhibitor both blocked in vivo tumor growth in a murine HCC xenograft model. High levels of HSP90 and DDX5 protein were associated with poor prognoses. Conclusions: HSP90 interacted with DDX5 protein and subsequently protected DDX5 protein from AMPK/ULK1-regulated autophagic degradation. DDX5 and HSP90 are therefore potential therapeutic targets for HCC.Item Improved understanding of the spatially-heterogeneous relationship between satellite solar-induced chlorophyll fluorescence and ecosystem productivity(Elsevier, 2021-10) Song, Yang; Wang, Lixin; Wang, Jing; Earth Science, School of ScienceSatellite solar-induced chlorophyll fluorescence (SIF) is deemed as a good proxy for vegetation photosynthesis. To date, SIF has been shown to correlate strongly with gross primary productivity (GPP) at ecosystem scale and perform well in monitoring the impacts of extreme climate events on ecosystem productivity. However, the SIF-GPP relationship exhibits a spatially-heterogeneous pattern across ecosystems and produces both linear and nonlinear results at different spatiotemporal scales. Understanding of the different spatiotemporal SIF-GPP relationships is still incomplete and somewhat controversial in previous studies. Here, based on the light-use efficiency (LUE) models, this study investigated the spatially-heterogeneous SIF-GPP relationships across the conterminous United States (CONUS), and examined the possible drivers and mechanisms. Our results showed that SIF and GPP exhibited similar spatiotemporal patterns but responded differently to environmental factors (i.e., soil moisture, precipitation, photosynthetically active radiation, air temperature, and atmospheric vapor pressure deficit). The correlation analysis showed that the SIF-GPP relationships were spatially-heterogeneous across the CONUS both at monthly and annual scales. Moreover, our findings also indicated that different biome types could partly explain the spatial heterogeneity of SIF-GPP relationship. Different canopy structures and vegetation coverages across biomes could be primary drivers of the spatially-heterogeneous SIF-GPP relationship. In addition, the SIF-GPP relationships under the baseline and drought scenarios appeared to be similar and consistent. It implies that there could be an invariant SIF-GPP relationship under both drought and non-drought conditions, leading to a weak effect of interannual drought on the spatial heterogeneity. In summary, our results highlight that the effects of biome characteristics (Ωbiome) and environmental stresses (Φstress) on spatially-heterogeneous SIF-GPP relationship and further explore possible mechanisms of the linkage between SIF and GPP.Item Increased Global Vegetation Productivity Despite Rising Atmospheric Dryness Over the Last Two Decades(AGU, 2022-07) Song, Yang; Jiao, Wenzhe; Wang, Jing; Wang, Lixin; Earth and Environmental Sciences, School of ScienceRising atmospheric dryness [vapor pressure deficit (VPD)] can limit photosynthesis and thus reduce vegetation productivity. Meanwhile, plants can benefit from global warming and the fertilization effect of carbon dioxide (CO2). There are growing interests to study climate change impacts on terrestrial vegetation. However, global vegetation productivity responses to recent climate and CO2 trends remain to be fully understood. Here, we provide a comprehensive evaluation of the relative impacts of VPD, temperature, and atmospheric CO2 concentration on global vegetation productivity over the last two decades using a robust ensemble of solar-induced chlorophyll fluorescence (SIF) and gross primary productivity (GPP) data. We document a significant increase in global vegetation productivity with rising VPD, temperature, and atmospheric CO2 concentration over this period. For global SIF (or GPP), the decrease due to rising VPD was comparable to the increase due to warming but far less than the increase due to elevated CO2 concentration. We found that rising VPD counteracted only a small proportion (approximately 8.1%–15.0%) of the warming and CO2-induced increase in global SIF (or GPP). Despite the sharp rise in atmospheric dryness imposing a negative impact on plants, the warming and CO2 fertilization effects contributed to a persistent and widespread increase in vegetation productivity over the majority (approximately 66.5%–72.2%) of the globally vegetated areas. Overall, our findings provide a quantitative and comprehensive attribution of rising atmospheric dryness on global vegetation productivity under concurrent climate warming and CO2 increasing.Item Intermediate MCAD Deficiency Associated with a Novel Mutation of the ACADM Gene: c.1052C>T(Hindawi, 2015) Drendel, Holli M.; Pike, Jason E.; Schumacher, Katherine; Ouyang, Karen; Wang, Jing; Stuy, Mary; Dlouhy, Stephen; Bai, Shaochun; Department of Medical and Molecular Genetics, IU School of MedicineMedium-chain acyl-CoA dehydrogenase deficiency (MCADD) is an autosomal recessive disorder that leads to a defect in fatty acid oxidation. ACADM is the only candidate gene causing MCAD deficiency. A single nucleotide change, c.985A>G, occurring at exon 11 of the ACADM gene, is the most prevalent mutation. In this study, we report a Caucasian family with multiple MCADD individuals. DNA sequence analysis of the ACADM gene performed in this family revealed that two family members showing mild MCADD symptoms share the same novel change in exon 11, c.1052C>T, resulting in a threonine-to-isoleucine change. The replacement is a nonconservative amino acid change that occurs in the C-terminal all-alpha domain of the MCAD protein. Here we report the finding of a novel missense mutation, c.1052C>T (p.Thr326Ile), in the ACADM gene. To our knowledge, c.1052C>T has not been previously reported in the literature or in any of the current databases we utilize. We hypothesize that this particular mutation in combination with p.Lys304Glu results in an intermediate clinical phenotype of MCADD.Item Materials Development in Teaching Chinese as a Foreign Language(Office of the Vice Chancellor for Research, 2015-04-17) Wang, JingMaterials development usually consumes a lot of money and effort, and therefore it deserves great attention. It is even more important to study the subject in the field of teaching Chinese as a foreign language (CFL) because limited research has been carried out. Professionals in the CFL field have noticed the following phenomenon: On the one hand, many new textbooks appear on the market every year; on the other hand, instructors of the Chinese language still find it difficult to get the ideal textbooks for their students. This presentation aims to reveal perspectives from expert textbook writers. Four expert textbook writers participated in the study, and each was interviewed for an hour. A qualitative method of grounded theory was used to analyze the interview data, and four themes emerged from the data. This presentation discusses the themes and provides pedagogical applications of the findings.Item The novel ZIP4 regulation and its role in ovarian cancer(Impact Journals, 2017-09-30) Fan, Qipeng; Cai, Qingchun; Li, Pengfei; Wang, Wenyan; Wang, Jing; Gerry, Emily; Wang, Tian-Li; Shih, Ie-Ming; Nephew, Kenneth P.; Xu, Yan; Obstetrics and Gynecology, School of MedicineOur RNAseq analyses revealed that ZIP4 is a top gene up-regulated in more aggressive ovarian cancer cells. ZIP4's role in cancer stem cells has not been reported in any type of cancer. In addition, the role and regulation of ZIP4, a zinc transporter, have been studied in the context of extracellular zinc transporting. Factors other than zinc with ZIP4 regulatory effects are essentially unknown. ZIP4 expression and its regulation in epithelial ovarian cancer cells was assessed by immunoblotting, quantitative PCR, or immunohistochemistry staining in human ovarian tissues. Cancer stem cell-related activities were examined to evaluate the role of ZIP4 in human high-grade serous ovarian cancer cells in vitro and in vivo. RNAi and CRISPR techniques were used to knockdown or knockout ZIP4 and related genes. Ovarian cancer tissues overexpressed ZIP4 when compared with normal and benign tissues. ZIP4 knockout significantly reduced several cancer stem cell-related activities in EOC cells, including proliferation, anoikis-resistance, colony-formation, spheroid-formation, drug-resistance, and side-population in vitro. ZIP4-expressing side-population highly expressed known CSC markers ALDH1 and OCT4. ZIP4 knockout dramatically reduced tumorigenesis and ZIP4 overexpression increased tumorigenesis in vivo. In addition, the ZIP4-expressing side-population had the tumor initiating activity. Moreover, the oncolipid lysophosphatic acid effectively up-regulated ZIP4 expression via the nuclear receptor peroxisome proliferator-activated receptor gamma and lysophosphatic acid 's promoting effects in cancer stem cell-related activities in HGSOC cells was at least partially mediated by ZIP4 in an extracellular zinc-independent manner. Our critical data imply that ZIP4 is a new and important cancer stem cell regulator in ovarian cancer. Our data also provide an innovative interpretation for the apparent disconnection between low levels of zinc and up-regulation of ZIP4 in ovarian cancer tissues.