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\"This comprehensive text covers the history of women and gender in Japan, Korea, and China in the early modern and modern eras by examining the dynamic histories of sexuality; gender ideology, discourse, and legal construction; marriage and the family; and the gendering of work, society, and power. The authors take the unique approach of locating gender history within a society's national history as well as describing its role in an integrated history of East Asia. In addition, this book examines the global context of historical changes in these countries and highlights cross-cultural themes that transcend national boundaries. For example, themes or concepts such as \"writing,\" \"the body,\" \"feminism,\" \"immigration and diasporas,\" and \"Confucianism\" are part of an integrated history. The authors capture the flow of ideas, people, materials, and texts throughout these three countries in an easily accessible way for students\"-- Provided by publisher.

Kikuchi-Fujimoto disease (KFD) is a rare entity characterized by subacute necrotizing lymphadenopathy and frequently associated with fever. Young adults of Asian ancestry are most commonly affected, but it has been reported worldwide. Despite many studies in the literature, the cause of KFD remains uncertain. Histologically, KFD is characterized by paracortical lymph node expansion with patchy, well-circumscribed areas of necrosis showing abundant karyorrhectic nuclear debris and absence of neutrophils and eosinophils. Three evolving histologic patterns—proliferative, necrotizing, and xanthomatous—have been recognized. By immunohistochemistry, histiocytes in KFD are positive for myeloperoxidase. There is a marked predominance of T cells in the lesions (with mostly CD8-positive cells) with very few B cells. The differential diagnosis of KFD includes infectious lymphadenitis, autoimmune lymphadenopathy (primarily systemic lupus erythematosus), and lymphoma. Clinicians and pathologists are poorly familiar with this entity, which frequently causes significant diagnostic challenges.

Acute respiratory distress syndrome (ARDS), a life-threatening condition characterized by hypoxemia and poor lung compliance, is associated with high mortality. ARDS induced by COVID-19 has similar clinical presentations and pathological manifestations as non-COVID-19 ARDS. However, COVID-19 ARDS is associated with a more protracted inflammatory respiratory failure compared to traditional ARDS. Therefore, a comprehensive molecular comparison of ARDS of different etiologies groups may pave the way for more specific clinical interventions. In this study, we compared COVID-19 ARDS (n = 43) and bacterial sepsis-induced (non-COVID-19) ARDS (n = 24) using multi-omic plasma profiles covering 663 metabolites, 1,051 lipids, and 266 proteins. To address both between- and within- ARDS group variabilities we followed two approaches. First, we identified 706 molecules differently abundant between the two ARDS etiologies, revealing more than 40 biological processes differently regulated between the two groups. From these processes, we assembled a cascade of therapeutically relevant pathways downstream of sphingosine metabolism. The analysis suggests a possible overactivation of arginine metabolism involved in long-term sequelae of ARDS and highlights the potential of JAK inhibitors to improve outcomes in bacterial sepsis-induced ARDS. The second part of our study involved the comparison of the two ARDS groups with respect to clinical manifestations. Using a data-driven multi-omic network, we identified signatures of acute kidney injury (AKI) and thrombocytosis within each ARDS group. The AKI-associated network implicated mitochondrial dysregulation which might lead to post-ARDS renal-sequalae. The thrombocytosis-associated network hinted at a synergy between prothrombotic processes, namely IL-17, MAPK, TNF signaling pathways, and cell adhesion molecules. Thus, we speculate that combination therapy targeting two or more of these processes may ameliorate thrombocytosis-mediated hypercoagulation. We present a first comprehensive molecular characterization of differences between two ARDS etiologies-COVID-19 and bacterial sepsis. Further investigation into the identified pathways will lead to a better understanding of the pathophysiological processes, potentially enabling novel therapeutic interventions.

In a quantum dot in the Kondo regime, electrical charges are effectively frozen, but the quantum dot remains electrically conducting owing to strong electron–electron correlations. Conduction from a frozen charge A central theme in condensed matter physics is the understanding of many-body electron–electron interactions, and nanoscale devices enable us to study the underlying principles at the single-electron level. Matthieu Desjardins et al . reveal a remarkable electron–electron interaction effect by examining a carbon nanotube quantum dot placed within a microwave circuit. They tune the quantum dot to the Kondo regime—an archetype of strong electronic correlations—and use combined electronic and microwave measurements to show that, even though electrical charges are effectively frozen because tunnelling of electrons into the dot is not possible, the dot remains electronically conducting. This is due to the strong Kondo correlations. The authors suggest that their measurement platform could be a useful tool for probing charge dynamics in a range of other correlated systems. The ability to control electronic states at the nanoscale has contributed to our modern understanding of condensed matter. In particular, quantum dot circuits represent model systems for the study of strong electronic correlations, epitomized by the Kondo effect 1 , 2 , 3 . We use circuit quantum electrodynamics architectures to study the internal degrees of freedom of this many-body phenomenon. Specifically, we couple a quantum dot to a high-quality-factor microwave cavity to measure with exceptional sensitivity the dot’s electronic compressibility, that is, its ability to accommodate charges. Because electronic compressibility corresponds solely to the charge response of the electronic system, it is not equivalent to the conductance, which generally involves other degrees of freedom such as spin. Here, by performing dual conductance and compressibility measurements in the Kondo regime, we uncover directly the charge dynamics of this peculiar mechanism of electron transfer. The Kondo resonance, visible in transport measurements, is found to be ‘transparent’ to microwave photons trapped in the high-quality cavity, thereby revealing that (in such a many-body resonance) finite conduction is achieved from a charge frozen by Coulomb interaction. This freezing of charge dynamics 4 , 5 , 6 is in contrast to the physics of a free electron gas. We anticipate that the tools of cavity quantum electrodynamics could be used in other types of mesoscopic circuits with many-body correlations 7 , 8 , providing a model system in which to perform quantum simulation of fermion–boson problems.

Nuclear fusion is one of the most attractive alternatives to carbon-dependent energy sources 1 . Harnessing energy from nuclear fusion in a large reactor scale, however, still presents many scientific challenges despite the many years of research and steady advances in magnetic confinement approaches. State-of-the-art magnetic fusion devices cannot yet achieve a sustainable fusion performance, which requires a high temperature above 100 million kelvin and sufficient control of instabilities to ensure steady-state operation on the order of tens of seconds 2 , 3 . Here we report experiments at the Korea Superconducting Tokamak Advanced Research 4 device producing a plasma fusion regime that satisfies most of the above requirements: thanks to abundant fast ions stabilizing the core plasma turbulence, we generate plasmas at a temperature of 100 million kelvin lasting up to 20 seconds without plasma edge instabilities or impurity accumulation. A low plasma density combined with a moderate input power for operation is key to establishing this regime by preserving a high fraction of fast ions. This regime is rarely subject to disruption and can be sustained reliably even without a sophisticated control, and thus represents a promising path towards commercial fusion reactors. A magnetic confinement regime established at the Korea Superconducting Tokamak Advanced Research device enables the generation of plasmas over 10 8  kelvin for 20 seconds with the aid of fast ions without plasma edge instabilities or impurity accumulation.

Accumulating evidence illustrates a fundamental role for mitochondria in lung alveolar type 2 epithelial cell (AEC2) dysfunction in the pathogenesis of idiopathic pulmonary fibrosis. However, the role of mitochondrial fusion in AEC2 function and lung fibrosis development remains unknown. Here we report that the absence of the mitochondrial fusion proteins mitofusin1 (MFN1) and mitofusin2 (MFN2) in murine AEC2 cells leads to morbidity and mortality associated with spontaneous lung fibrosis. We uncover a crucial role for MFN1 and MFN2 in the production of surfactant lipids with MFN1 and MFN2 regulating the synthesis of phospholipids and cholesterol in AEC2 cells. Loss of MFN1, MFN2 or inhibiting lipid synthesis via fatty acid synthase deficiency in AEC2 cells exacerbates bleomycin-induced lung fibrosis. We propose a tenet that mitochondrial fusion and lipid metabolism are tightly linked to regulate AEC2 cell injury and subsequent fibrotic remodeling in the lung. Mitochondria of alveolar type 2 epithelial cells (AEC2) in the lung have been suggested to play a role in the development of idiopathic pulmonary fibrosis (IPF). Here the authors show that loss of mitofusin1 and mitofusin2 in murine AEC2 cells leads to the development of lung fibrosis through the regulation of surfactant lipids.

Increasing evidence has shown that Coronavirus disease 19 (COVID-19) severity is driven by a dysregulated immunologic response. We aimed to assess the differences in inflammatory cytokines in COVID-19 patients compared to contemporaneously hospitalized controls and then analyze the relationship between these cytokines and the development of Acute Respiratory Distress Syndrome (ARDS), Acute Kidney Injury (AKI) and mortality. In this cohort study of hospitalized patients, done between March third, 2020 and April first, 2020 at a quaternary referral center in New York City we included adult hospitalized patients with COVID-19 and negative controls. Serum specimens were obtained on the first, second, and third hospital day and cytokines were measured by Luminex. Autopsies of nine cohort patients were examined. We identified 90 COVID-19 patients and 51 controls. Analysis of 48 inflammatory cytokines revealed upregulation of macrophage induced chemokines, T-cell related interleukines and stromal cell producing cytokines in COVID-19 patients compared to the controls. Moreover, distinctive cytokine signatures predicted the development of ARDS, AKI and mortality in COVID-19 patients. Specifically, macrophage-associated cytokines predicted ARDS, T cell immunity related cytokines predicted AKI and mortality was associated with cytokines of activated immune pathways, of which IL-13 was universally correlated with ARDS, AKI and mortality. Histopathological examination of the autopsies showed diffuse alveolar damage with significant mononuclear inflammatory cell infiltration. Additionally, the kidneys demonstrated glomerular sclerosis, tubulointerstitial lymphocyte infiltration and cortical and medullary atrophy. These patterns of cytokine expression offer insight into the pathogenesis of COVID-19 disease, its severity, and subsequent lung and kidney injury suggesting more targeted treatment strategies.

Making strides with DNA DNA is the construction material of choice for self-assembling nanostructures, but most examples of its use have focused on specific targets, rather than aspiring to the versatility achieved in nature. Yin et al . take a step towards versatility with a new system, based on modular DNA 'hairpins', that allows assembly and disassembly pathways to be programmed into DNA building blocks. Key to the new protocol is the 'reaction graph', a simple representation of DNA modules and their interactions that simplifies the overall design process. This allows assembly programs to prepare branched junction molecules, self-catalysing pairs of DNA duplexes, molecular trees and a bipedal molecule that walks along a DNA track. A versatile system, based on modular DNA hairpins, that allows assembly and disassembly pathways to be programmed into DNA building blocks is described. A key development is the reaction graph, a simple representation of DNA modules and their interactions that simplifies the overall design process. In this way, it is possible to write assembly programs that are executed to prepare branched junction molecules, self-catalysing pairs of DNA duplexes and molecular trees. In nature, self-assembling and disassembling complexes of proteins and nucleic acids bound to a variety of ligands perform intricate and diverse dynamic functions. In contrast, attempts to rationally encode structure and function into synthetic amino acid and nucleic acid sequences have largely focused on engineering molecules that self-assemble into prescribed target structures, rather than on engineering transient system dynamics 1 , 2 . To design systems that perform dynamic functions without human intervention, it is necessary to encode within the biopolymer sequences the reaction pathways by which self-assembly occurs. Nucleic acids show promise as a design medium for engineering dynamic functions, including catalytic hybridization 3 , 4 , 5 , 6 , triggered self-assembly 7 and molecular computation 8 , 9 . Here, we program diverse molecular self-assembly and disassembly pathways using a ‘reaction graph’ abstraction to specify complementarity relationships between modular domains in a versatile DNA hairpin motif. Molecular programs are executed for a variety of dynamic functions: catalytic formation of branched junctions, autocatalytic duplex formation by a cross-catalytic circuit, nucleated dendritic growth of a binary molecular ‘tree’, and autonomous locomotion of a bipedal walker.

Autophagy is a dynamic process by which cytosolic material, including organelles, proteins, and pathogens, are sequestered into membrane vesicles called autophagosomes, and then delivered to the lysosome for degradation. By recycling cellular components, this process provides a mechanism for adaptation to starvation. The regulation of autophagy by nutrient signals involves a complex network of proteins that include mammalian target of rapamycin, the class III phosphatidylinositol-3 kinase/Beclin 1 complex, and two ubiquitin-like conjugation systems. Additionally, autophagy, which can be induced by multiple forms of chemical and physical stress, including endoplasmic reticulum stress, and hypoxia, plays an integral role in the mammalian stress response. Recent studies indicate that, in addition to bulk assimilation of cytosol, autophagy may proceed through selective pathways that target distinct cargoes to autophagosomes. The principle homeostatic functions of autophagy include the selective clearance of aggregated protein to preserve proteostasis, and the selective removal of dysfunctional mitochondria (mitophagy). Additionally, autophagy plays a central role in innate and adaptive immunity, with diverse functions such as regulation of inflammatory responses, antigen presentation, and pathogen clearance. Autophagy can preserve cellular function in a wide variety of tissue injury and disease states, however, maladaptive or pro-pathogenic outcomes have also been described. Among the many diseases where autophagy may play a role include proteopathies which involve aberrant accumulation of proteins (e.g., neurodegenerative disorders), infectious diseases, and metabolic disorders such as diabetes and metabolic syndrome. Targeting the autophagy pathway and its regulatory components may eventually lead to the development of therapeutics.