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2,995 result(s) for "Kim, Ji-Eun"
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Reading in the digital age: young children's experiences with e-books : international studies with e-books in diverse contexts
This edited book focuses on affordances and limitations of e-books for early language and literacy, features and design of e-books for early language and literacy, print versus e-books in early language and literacy development, and uses of and guidelines for how to use e-books in school and home literacy practices. Uniquely, this book includes critical reviews of diverse aspects of e-books (e.g., features) and e-book uses (e.g., independent reading) for early literacy as well as multiple examinations of e-books in home and school contexts using a variety of research methods and/or theoretical frames. The studies of childrens engagement with diverse types of e-books in different social contexts provide readers with a contemporary and comprehensive understanding of this topic. Research has demonstrated that ever-increasing numbers of children use digital devices as part of their daily routine. Yet, despite childrens frequent use of e-books from an early age, there is a limited understanding regarding how those e-books are actually being used at home and school. As more e-books become available, it is important to examine the educational benefits and limitations of different types of e-books for children. So far, studies on the topic have presented inconsistent findings regarding potential benefits and limitations of e-books for early literacy activities (e.g., independent reading, shared reading). The studies in this book aim to fill such gaps in the literature.
The Roles and Associated Mechanisms of Adipokines in Development of Metabolic Syndrome
Metabolic syndrome is a cluster of metabolic indicators that increase the risk of diabetes and cardiovascular diseases. Visceral obesity and factors derived from altered adipose tissue, adipokines, play critical roles in the development of metabolic syndrome. Although the adipokines leptin and adiponectin improve insulin sensitivity, others contribute to the development of glucose intolerance, including visfatin, fetuin-A, resistin, and plasminogen activator inhibitor-1 (PAI-1). Leptin and adiponectin increase fatty acid oxidation, prevent foam cell formation, and improve lipid metabolism, while visfatin, fetuin-A, PAI-1, and resistin have pro-atherogenic properties. In this review, we briefly summarize the role of various adipokines in the development of metabolic syndrome, focusing on glucose homeostasis and lipid metabolism.
Cancer cell–induced neutrophil extracellular traps promote both hypercoagulability and cancer progression
Neutrophils can generate extracellular net-like structures by releasing their DNA-histone complexes and antimicrobial peptides, which is called neutrophil extracellular traps (NETs). Various stimuli can induce NET formation. In particular, neutrophils and NET formation are abundant in tumor tissue. This study investigated how cancer cells induce NET formation and whether this NET formation promotes plasma thrombin generation and cancer progression. Induction of NET formation by a pancreatic cancer cell line (AsPC-1) was assessed by measuring the histone-DNA complex level. The endogenous thrombin potential (ETP) was measured by thrombin generation assay. In vitro migration, invasion, and tubule formation assays were performed. The circulating levels of NET markers and hypercoagulability markers were assessed in 62 patients with pancreatobiliary malignancy and 30 healthy controls. AsPC-1 significantly induced NET formation in a dose-dependent manner. Conditioned medium (CM) from AsPC-1 also induced NETs. Interestingly, NET-formation was abolished by heat-inactivated CM, but not by lipid-extracted CM, suggesting an important role of protein components. A reactive oxygen species inhibitor did not inhibit cancer cell-induced NET formation, but prostaglandin E1 (PGE1, cyclic adenosine monophosphate inducer) and antithrombin did. NETs significantly increased ETP of normal plasma. Of note, NETs promoted cancer cell migration and invasion as well as angiogenesis, which were inhibited by histone-binding agents (heparin, polysialic acid), a DNA-degrading enzyme, and Toll-like receptor neutralizing antibodies. In patients with pancreatobiliary malignancy, elevated NET markers correlated well with hypercoagulability makers. Our findings indicate that cancer cell-induced NET formation enhances both hypercoagulability and cancer progression and suggest that inhibitors of NET formation such as PGE1 and antithrombin can be potential therapeutics to reduce both hypercoagulability and cancer progression.
Advanced zinc-air batteries based on high-performance hybrid electrocatalysts
Primary and rechargeable Zn-air batteries could be ideal energy storage devices with high energy and power density, high safety and economic viability. Active and durable electrocatalysts on the cathode side are required to catalyse oxygen reduction reaction during discharge and oxygen evolution reaction during charge for rechargeable batteries. Here we developed advanced primary and rechargeable Zn-air batteries with novel CoO/carbon nanotube hybrid oxygen reduction catalyst and Ni-Fe-layered double hydroxide oxygen evolution catalyst for the cathode. These catalysts exhibited higher catalytic activity and durability in concentrated alkaline electrolytes than precious metal Pt and Ir catalysts. The resulting primary Zn-air battery showed high discharge peak power density ~265 mW cm −2 , current density ~200 mA cm −2 at 1 V and energy density >700 Wh kg −1 . Rechargeable Zn-air batteries in a tri-electrode configuration exhibited an unprecedented small charge–discharge voltage polarization of ~0.70 V at 20 mA cm −2 , high reversibility and stability over long charge and discharge cycles. Metal-air batteries are promising for energy storage because of their high theoretical energy density, but their realization is hampered by the lack of efficient and robust air catalysts. Li et al . construct stable zinc-air batteries using novel catalysts for oxygen reduction and evolution reactions.
Ubiquity of human-induced changes in climate variability
While climate change mitigation targets necessarily concern maximum mean state changes, understanding impacts and developing adaptation strategies will be largely contingent on how climate variability responds to increasing anthropogenic perturbations. Thus far Earth system modeling efforts have primarily focused on projected mean state changes and the sensitivity of specific modes of climate variability, such as the El Niño–Southern Oscillation. However, our knowledge of forced changes in the overall spectrum of climate variability and higher-order statistics is relatively limited. Here we present a new 100-member large ensemble of climate change projections conducted with the Community Earth System Model version 2 over 1850–2100 to examine the sensitivity of internal climate fluctuations to greenhouse warming. Our unprecedented simulations reveal that changes in variability, considered broadly in terms of probability distribution, amplitude, frequency, phasing, and patterns, are ubiquitous and span a wide range of physical and ecosystem variables across many spatial and temporal scales. Greenhouse warming in the model alters variance spectra of Earth system variables that are characterized by non-Gaussian probability distributions, such as rainfall, primary production, or fire occurrence. Our modeling results have important implications for climate adaptation efforts, resource management, seasonal predictions, and assessing potential stressors for terrestrial and marine ecosystems.
Bioenergetic state regulates innate inflammatory responses through the transcriptional co-repressor CtBP
The innate inflammatory response contributes to secondary injury in brain trauma and other disorders. Metabolic factors such as caloric restriction, ketogenic diet, and hyperglycemia influence the inflammatory response, but how this occurs is unclear. Here, we show that glucose metabolism regulates pro-inflammatory NF-κB transcriptional activity through effects on the cytosolic NADH:NAD + ratio and the NAD(H) sensitive transcriptional co-repressor CtBP. Reduced glucose availability reduces the NADH:NAD + ratio, NF-κB transcriptional activity, and pro-inflammatory gene expression in macrophages and microglia. These effects are inhibited by forced elevation of NADH, reduced expression of CtBP, or transfection with an NAD(H) insensitive CtBP, and are replicated by a synthetic peptide that inhibits CtBP dimerization. Changes in the NADH:NAD + ratio regulate CtBP binding to the acetyltransferase p300, and regulate binding of p300 and the transcription factor NF-κB to pro-inflammatory gene promoters. These findings identify a mechanism by which alterations in cellular glucose metabolism can influence cellular inflammatory responses. Several metabolic factors affect cellular glucose metabolism as well as the innate inflammatory response. Here, the authors show that glucose metabolism regulates pro-inflammatory responses through effects on the cytosolic NADH:NAD+ ratio and the NAD(H)-sensitive transcription co-repressor CtBP.
Digital Health Intervention Effect on Older Adults With Chronic Diseases Living Alone: Systematic Review and Meta-Analysis of Randomized Controlled Trials
The incidence of chronic diseases is increasing owing to the aging population; in particular, older adults living alone struggle with self-management and medical expenses. Digital health can contribute to medical cost management and health promotion, but its effectiveness for older adults living alone remains unclear. In a rapidly aging society, it is important to demonstrate the effect of digital health on improving the lives of older adults living alone and reducing the burden of chronic diseases. This study aims to examine the intervention effects of digital health on self-management, quality of life, and medical factors for older adults living alone with common chronic diseases such as cardiovascular disease, respiratory disease, and musculoskeletal disorders through a systematic literature review and meta-analysis. We searched the literature using 3 databases, including PubMed, CINAHL, and Cochrane CENTRAL, for literature published in overseas academic journals up to October 2024. The final 11 papers were used for analysis based on selection and exclusion criteria. Meta-analysis was used to calculate the mean difference and standardized mean difference (SMD) for the selected literature using RevMan (version 5.4; Cochrane). The effect size and heterogeneity were calculated through 95% CI. As a result of conducting a meta-analysis of 8 of 11 documents, there was a significant effect of self-management factors on moderate-to-vigorous physical activity (SMD=0.08; z=2.07; P=.04). However, among self-management factors, low-density lipoprotein cholesterol (SMD=-0.04; z=0.91; P=.36) did not show statistically significant results. Among the medical factors, general quality of life (SMD=0.11; z=0.93; P=.35), depression (SMD=-3.95; z=1.59; P=.11), and hospital days (SMD=-1.57; z=0.91; P=.36) also did not show statistically significant results. However, it was confirmed that they improved after a digital health intervention. This study demonstrated that digital health interventions are effective in improving physical activity in older adults with chronic diseases living alone. However, owing to the characteristics of older adults living alone, there is a need to further expand digital health to combine care services that can manage diseases at home.
Gut commensal Kineothrix alysoides mitigates liver dysfunction by restoring lipid metabolism and gut microbial balance
Metabolic dysfunction-associated steatotic liver disease (MASLD), previously known as Non-Alcoholic Fatty Liver Disease, is a widespread liver condition characterized by excessive fat buildup in hepatocytes without significant alcohol consumption. Manipulation of the gut microbiome has been considered to prevent and improve the occurrence and progression of MASLD, particularly through the gut-liver axis. This study aimed to investigate the correlation between the gut microbiome and liver function and determine whether the gut microbiome can ameliorate MASLD. We comparatively analyzed the gut microbiome composition between mice fed normal chow and those fed a high-fat diet and observed that the abundance of Kineothrix alysoides decreased in the high-fat group. Further analysis showed that treatment with K. alysoides in the high-fat diet group led to decreased weight loss, and MASLD attenuation. Importantly, K. alysoides treatment attenuated MASLD in mice fed a high-fat, high-fructose diet (HFHF), which can cause advanced liver damage. Furthermore, administration of K. alysoides altered the gut microbial composition in the HFHF diet group and improved MASLD. Overall, these findings demonstrate the potential of K. alysoides in restoring gut health and facilitating lipid metabolism to prevent and treat MASLD.
Core Dynamics of the MJO
The Madden–Julian oscillation (MJO) is a large-scale eastward-moving system that dominates tropical subseasonal perturbations with far-reaching impacts on global weather–climate. For nearly a half century since its discovery, there has not been a consensus on the most fundamental dynamics of the MJO, despite intensive studies with a number of theories proposed. In this study, using a simple analytical approach, we found a solution to the linear equatorial shallow-water equations with momentum damping that resembles a harmonic oscillator. This solution exhibits the key characteristics of the observed MJO: its intraseasonal periodicity at the planetary scale and eastward propagation. In contrast to theories that interpret the MJO as a new mode of variability emerging from the evolution in moisture, our solution emphasizes that the core of the MJO resides in the dynamics without explicit fluctuations in moisture. Moisture still plays a role in supplying energy to the core dynamics of the MJO, and determining the value of the equivalent depth required by the theory. The energy source may come from stochastic forcing in the tropics or from the extratropics. The scale selection for the MJO comes from scale-dependent responses to scale-independent Rayleigh damping. We also demonstrate that the MJO solution introduced here reproduces the observed swallowtail structure and the phase relation between zonal wind and geopotential of the MJO, and the continuum nature of the transition between the MJO and Kelvin waves. Roles of feedback mechanisms in the MJO are also discussed using the same simple mathematical framework.
Single cell and genetic analyses reveal conserved populations and signaling mechanisms of gastrointestinal stromal niches
Stomach and intestinal stem cells are located in discrete niches called the isthmus and crypt, respectively. Recent studies have demonstrated a surprisingly conserved role for Wnt signaling in gastrointestinal development. Although intestinal stromal cells secrete Wnt ligands to promote stem cell renewal, the source of stomach Wnt ligands is still unclear. Here, by performing single cell analysis, we identify gastrointestinal stromal cell populations with transcriptome signatures that are conserved between the stomach and intestine. In close proximity to epithelial cells, these perictye-like cells highly express telocyte and pericyte markers as well as Wnt ligands, and they are enriched for Hh signaling. By analyzing mice activated for Hh signaling, we show a conserved mechanism of GLI2 activation of Wnt ligands. Moreover, genetic inhibition of Wnt secretion in perictye-like stromal cells or stromal cells more broadly demonstrates their essential roles in gastrointestinal regeneration and development, respectively, highlighting a redundancy in gastrointestinal stem cell niches. Wnt signals for intestinal stem cell self-renewal originate from the stroma and Paneth cells, but the source in stomach is unclear. Here the authors identify a conserved population of stromal cells adjacent to stomach epithelia where Gli2 activates Wnt ligands to promote gastrointestinal regeneration and development.