• 한국언어정보학회지:언어와정보
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• 제7권1호
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• pp.87-99
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• 2003

This paper investigates the role of input frequency in the acquisition of verb argument structures based on distributional information of a corpus of utterances derived from the English CHILDES database (MacWhinney 1993). It has been widely accepted that children successfully learn verb argument structures by innate language mechanisms, such as linking rules which connect verb meanings and its syntactic structures. In contrast, an approach to language acquisition called “statistical language learning” has currently claimed that children could succeed in acquiring syntactic structures in the absence of innate language mechanisms, making use of distributional properties of the input. In this paper, I evaluate the feasibility of the statistical learning in acquiring verb argument structures, based on distributional information about locative verbs in parental input. The naturalistic data allow us to investigate to what extent the statistical learning approach can and cannot help children succeed in learning the syntax of locative verbs. Based on the results of English database analysis, I show that there is rich statistical information for learning the syntactic possibilities of locative verbs in parental input, despite some limitations in the statistical learning approach.

• Journal of Periodontal and Implant Science
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• 제43권1호
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• pp.3-11
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• 2013

Periodontitis is a chronic inflammation of periodontal tissue caused by subgingival plaque-associated bacteria. Periodontitis has long been understood to be the result of an excessive host response to plaque bacteria. In addition, periodontal pathogens have been regarded as the causative agents that induce a hyperinflammatory response from the host. In this brief review, host-microbe interaction of nonperiodontopathic versus periodontopathic bacteria with innate immune components encountered in the gingival sulcus will be described. In particular, we will describe the susceptibility of these microbes to antimicrobial peptides (AMPs) and phagocytosis by neutrophils, the induction of tissue-destructive mediators from neutrophils, the induction of AMPs and interleukin (IL)-8 from gingival epithelial cells, and the pattern recognition receptors that mediate the regulation of AMPs and IL-8 in gingival epithelial cells. This review indicates that true periodontal pathogens are poor activators/suppressors of a host immune response, and they evade host defense mechanisms.

• 셀메드
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• 제3권3호
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• pp.23.1-23.3
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• 2013

According to the traditional Korean medicine (TKM), kidney has been recognized as the roof of innate endowment because it plays an important role in the birth, growth, sexual reproduction, and aging. Kidney essence insufficiency syndrome (KEIS) is caused when kidney is impaired. KEIS is characterized by retarded development, decreased reproduction, tinnitus, loosening of teeth, and loss of hair and forgetfulness. In traditional Chinese medicine, KEIS mouse model was established by use of threatinjuring the kidney combined with over-fatigue. However, the TKM theory-based KEIS experiment model has not been described correctly. In the present study, we suggest a new KEIS experiment model including following cases; 1) weakness of father essence and mother blood, 2) life nurturing during pregnancy, 3) full-term gestation period.

• Asian-Australasian Journal of Animal Sciences
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• 제28권11호
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• pp.1519-1524
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• 2015

It is well known that prepartum sows have an innate motivation to build a nest before parturition. Under commercial conditions, however, the farrowing crate, which is widely used in modern pig husbandry, inhibits this innate behaviour through the lack of space, materials, or both. Thus, restriction of nest-building behaviour could generate increased stress, resulting in a decrease in maternal endogenous hormones. Hence, it could lead to detrimental effects on farrowing and lactating performance. Here we review interactions between prepartum nest-building behaviour, stress and maternal endogenous hormone levels, and discuss their effects on parturition, lactation, and welfare of sows and offspring.

• International Journal of Oral Biology
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• 제42권3호
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• pp.85-90
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• 2017

Mitochondria participate in various intracellular metabolic pathways such as generating intracellular ATP, synthesizing several essential molecules, regulating calcium homeostasis, and producing the cell's reactive oxygen species (ROS). Emerging studies have demonstrated newly discovered roles of mitochondria, which participate in the regulation of innate immune responses by modulating NLRP3 inflammasomes. Here, we review the recently proposed pathways to be involved in mitochondria-mediated regulation of inflammasome activation and inflammation: 1) mitochondrial ROS, 2) calcium mobilization, 3) nicotinamide adenine dinucleotide ($NAD^+$) reduction, 4) cardiolipin, 5) mitofusin, 6) mitochondrial DNA, 7) mitochondrial antiviral signaling protein. Furthermore, we highlight the significance of mitophagy as a negative regulator of mitochondrial damage and NLRP3 inflammasome activation, as potentially helpful therapeutic approaches which could potentially address uncontrolled inflammation.

• Animal cells and systems
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• 제13권1호
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• pp.1-8
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• 2009

Toll-like receptor (TLR) family proteins, type I transmembrane proteins, play a central role in human innate immune response by recognizing common structural patterns in diverse molecules from bacteria, viruses and fungi. Recently four structures of the TLR and ligand complexes have been determined by high resolution x-ray crystallographic technique. In this review we summarize reported structures of TLRs and their proposed activation mechanisms. The structures demonstrate that binding of agonistic ligands to the extracellular domains of TLRs induces homo- or heterodimerization of the receptors. Dimerization of the TLR extracellular domains brings their two C-termini into close proximity. This suggests a plausible mechanism of TLR activation: ligand induces dimerization of the extracellular domains, which enforces juxtaposition of intracellular signaling domains for recruitment of intracellular adaptor proteins for signal initiation.

• BMB Reports
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• 제41권4호
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• pp.267-277
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• 2008

Insects mount a robust innate immune response against a wide array of microbial pathogens. The hallmark of the Drosophila humoral immune response is the rapid production of anti-microbial peptides in the fat body and their release into the circulation. Two recognition and signaling cascades regulate expression of these antimicrobial peptide genes. The Toll pathway is activated by fungal and many Gram-positive bacterial infections, whereas the immune deficiency (IMD) pathway responds to Gram-negative bacteria. Recent work has shown that the intensity and duration of the Drosophila immune response is tightly regulated. As in mammals, hyperactivated immune responses are detrimental, and the proper down-modulation of immunity is critical for protective immunity and health. In order to keep the immune response properly modulated, the Toll and IMD pathways are controlled at multiple levels by a series of negative regulators. In this review, we focus on recent advances identifying and characterizing the negative regulators of these pathways.

• Journal of Plant Biotechnology
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• 제38권4호
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• pp.278-284
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• 2011

The CCR4-CAF1-NOT complex-mediated degradation of mRNA is a fundamental aspect of gene regulation in eukaryotes. We herein examined the role of AtCAF1 in the innate immune and wound responses of plants. Our results showed that overexpression of AtCAF1 significantly downregulated the transcript level of EFR but not FLS2 and BRI1, as well as abolished up-regulated expression pattern of EFR in response to wounding. Consistently, Agrobacteriummediated transient expression of GUS was highly enhanced in the transgenic plants overexpressing AtCAF. Furthermore, JA responsive genes were down-regulated by overexpression of AtCAF, causing the transgenic plants overexpressing AtCAF more susceptible to necrotrophic fungal pathogen, Botrytis cinerea. These results suggest that The CCR4-CAF1-NOT complex-mediated degradation of mRNA negatively regulates wounding-mediated disease resistance in Arabidopsis thaliana.

• BMB Reports
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• 제50권10호
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• pp.496-503
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• 2017

The human body loses several billions of cells daily. When cells die in vivo, the corpse of each dead cell is immediately cleared. Specifically, dead cells are efficiently recognized and cleared by multiple types of neighboring phagocytes. Early research on cell death focused more on molecular mechanisms of cell death regulation while the cellular corpses were merely considered cellular debris. However, it has come to light that various biological stimuli following cell death are important for immune regulation. Clearance of normal dead cells occurs silently in immune tolerance. Exogenous or mutated antigens of malignant or infected cells can initiate adaptive immunity, thereby inducing immunogenicity by adjuvant signals. Several pathogens and cancer cells have strategies to limit the adjuvant signals and escape immune surveillance. In this review, we present an overview of the mechanisms of dead cell clearance and its immune regulations.

• The Plant Pathology Journal
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• 제30권2호
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• pp.109-116
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• 2014

There are an increasing number of outbreaks of human pathogens related to fresh produce. Thus, the growth of human pathogens on plants should be explored. Human pathogens can survive under the harsh environments in plants, and can adhere and actively invade plants. Plant-associated microbiota or insects contribute to the survival and transmission of enteric pathogens in plants. Human enteric pathogens also trigger plant innate immunity, but some pathogens-such as Salmonella-can overcome this defense mechanism.