• BMB Reports
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• v.39 no.4
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• pp.371-376
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• 2006

Crustacean hyperglycemic hormone (CHH) plays a major role in controlling glucose level in the haemolymph and also triggers important events during molting and reproductive cycles. In Penaeus monodon, three types of CHH, namely Pem-CHH1, Pem-CHH2 and Pem-CHH3, have been previously characterized. In this study, mouse polyclonal antibody was raised against recombinant Pem-CHH1 that was expressed in Escherichia coli. The anti-Pem-CHH1 antibody recognized all three types of Pem-CHHs but did not cross-react with either related hormone, molt-inhibiting hormone of P. monodon, or unrelated human growth hormone. The hyperglycemic activity in the extract from the eyestalk neural tissues was significantly depleted after incubating with anti-Pem-CHH antibody. Direct injection of the antibody into shrimp caused about 30-50% reduction in the haemolymph glucose level. The result demonstrates the ability of anti-Pem-CHH1 antibody to deplete the activity of CHH in vivo, and thus provides a possibility of using anti-Pem-CHH1 antibody to inhibit the hormone activity as a strategy to modulate growth and reproduction in this species.

• Journal of Yeungnam Medical Science
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• v.30 no.1
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• pp.4-9
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• 2013

Leptin, a 16-kDa cytokine, is secreted by adipose tissue in response to the surplus of fat store. Thereby, the brain is informed about the body's energy status. In the hypothalamus, leptin triggers specific neuronal subpopulations (e.g., POMC and NPY neurons) and activates several intracellular signaling events, including the JAK/STAT, MAPK, PI3K, and mTOR pathway, which eventually translates into decreased food intake and increased energy expenditure. Leptin signal is inhibited by a feedback inhibitory pathway mediated by SOCS3. PTP1B involves another inhibitory pathway of leptin. Leptin potently promotes fat mass loss and body weight reduction in lean subjects. However, it is not widely used in the clinical field because of leptin resistance, which is a common feature of obesity characterized by hyperleptinemia and the failure of exogenous leptin administration to provide therapeutic benefit in rodents and humans. The potential mechanisms of leptin resistance include the following: 1) increases in circulating leptin-binding proteins, 2) reduced transport of leptin across the blood-brain barrier, 3) decreased leptin receptor-B (LRB), and/or 4) the provocation of processes that diminish cellular leptin signaling (inflammation, endoplasmic reticulum stress, feedback inhibition, etc.). Thus, interference of the cellular mechanisms that attenuate leptin signaling improves leptin action in cells and animal models, suggesting the potential utility of these processes as points of therapeutic intervention. Various experimental trials and compounds that improve leptin resistance are introduced in this paper.

• Childhood Kidney Diseases
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• v.12 no.1
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• pp.11-22
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• 2008

Telomeres consist of tandem guanine-thymine(G-T) repeats in most eukaryotic chromosomes. Human telomeres are predominantly linear, double stranded DNA as they ended in 30-200 nucleotides(bases,b) 3'-overhangs. In DNA replication, removal of the terminal RNA primer from the lagging strand results in a 3'-overhang of uncopied DNA. This is because of bidirectional DNA replication and specificity of unidirectional DNA polymerase. After the replication, parental and daughter DNA strands have unequal lengths due to a combination of the end-replication problem and end-processing events. The gradual chromosome shortening is observed in most somatic cells and eventually leads to cellular senescence. Telomere shortening could be a molecular clock that signals the replicative senescence. The shortening of telomeric ends of human chromosomes, leading to sudden growth arrest, triggers DNA instability as biological switches. In addition, telomere dysfunction may cause chronic allograft nephropathy or kidney cancers. The renal cell carcinoma(RCC) in women may be less aggressive and have less genomic instability than in man. Younger patients with telomere dysfunction are at a higher risk for RCC than older patients. Thus, telomeres maintain the integrity of the genome and are involved in cellular aging and cancer. By studying the telomeric DNA, we may characterize the genetic determinants in diseases and discover the tools in molecular medicine.

• Animal cells and systems
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• v.10 no.3
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• pp.115-120
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• 2006

Parkinson's disease (PD) is a neurodegenerative disease caused by selective degeneration of dopaminergic neurons in the substantia nigra. Mutations in ${\alpha}$-synuclein have been causally linked to the pathogenesis of hereditary PD. In addition, it is a major component of Lewy body found in the brains of sporadic cases as well. In the present study, we examined whether overexpression of wild type or PD-related mutant ${\alpha}$-synuclein induces unfolded protein response (UPR) and triggers the known signaling pathway of the resulting endoplasmic reticulum (ER) stress in SH-SY5Y cells. Overexpression of wild type, A30P, and A53T ${\alpha}$-synuclein all induced XBP-1 mRNA splicing, one of the late stage UPR events. However, activation of ER membrane kinases and upregulation of ER or cytoplsmic chaperones were not detected when ${\alpha}$-synuclein was overexpressed. However, basal level of cytoplsmic calcium was elevated in ${\alpha}$-synuclein-expressing cells. Our observation suggests that overexpression of ${\alpha}$-synuclein induces UPR independent of the known ER membrane kinase-mediated signaling pathway and induces ER stress by disturbing calcium homeostasis.

• Journal of the Korean Society of Safety
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• v.36 no.1
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• pp.56-63
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• 2021

The narrative texts of industrial accident reports help to identify accident risk factors. They relate the accident triggers to the sequence of events and the outcomes of an accident. Particularly, a set of related keywords in the context of the narrative can represent how the accident proceeded. Previous studies on text analytics for structuring accident reports have been limited to extracting individual keywords without context. We proposed a context-based analysis using a Natural Language Processing (NLP) algorithm to remedy this shortcoming. This study aims to apply Word2Vec of the NLP algorithm to extract adjacent keywords, known as word embedding, conducted by the neural network algorithm based on supervised learning. During processing, Word2Vec is conducted by adjacent keywords in narrative texts as inputs to achieve its supervised learning; keyword weights emerge as the vectors representing the degree of neighboring among keywords. Similar keyword weights mean that the keywords are closely arranged within sentences in the narrative text. Consequently, a set of keywords that have similar weights presents similar accidents. We extracted ten accident processes containing related keywords and used them to understand the risk factors determining how an accident proceeds. This information helps identify how a checklist for an accident report should be structured.

• Journal of Microbiology and Biotechnology
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• v.23 no.12
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• pp.1785-1790
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• 2013

The synthetic machinery of ATF4 (activating transcription factor 4) is activated in response to various stress conditions involved in nutrient restriction, endoplasmic reticulum homeostasis, and oxidation. Stress-induced inhibition of proteasome activity triggers the unfolded protein response and endoplasmic reticulum stress, where ATF4 is crucial for consequent biological events. In the current study, we showed that the $NAD^+$-dependent deacetylase, SIRT1, suppresses ATF4 synthesis during proteasome inhibition. SIRT1 depletion via transfection of specific siRNA into HeLa cells resulted in a significant increase in ATF4 protein, which was observed specifically in the presence of the proteasome inhibitor MG132. Consistent with SIRT1 depletion data, transient transfection of cells with SIRT1-overexpressing plasmid induced a decrease in the ATF4 protein level in the presence of MG132. Interestingly, however, ATF4 mRNA was not affected by SIRT1, even in the presence of MG132, indicating that SIRT1-induced suppression of ATF4 synthesis occurs under post-transcriptional control. Accordingly, we propose that SIRT1 serves as a negative regulator of ATF4 protein synthesis at the post-transcriptional level, which is observed during stress conditions, such as proteasome inhibition.

• Geophysics and Geophysical Exploration
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• v.18 no.1
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• pp.21-30
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• 2015

Induced seismicity has been observed in the relation with lots of anthropogenic influence and at variety of geological conditions over the last several decades. This paper reviews those induced earthquakes and compares with each other as well as with natural tectonic earthquakes. Hydraulic fracturing is commonly used to enhance the permeability through new cracks in the rock formation. The process triggers the induced seismicity, which can give crucial information on the fracture network and oil/gas migration. In the similar way, unintentionally induced events during the production procedure of the field, dam reservoir, minig activity, or wastewater injection can be used to give insight into various hydrodynamic processes and changes of reservoir properties at a various scales. The general conclusion summarizes the uncertainty or limitations of knowledge up to date and presents some issues to be dealt with in the future research.

• Economic and Environmental Geology
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• v.52 no.5
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• pp.471-484
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• 2019

Liquefaction occurs by a temporal loss of sediment strength as a consequence of increased pore water pressure during the re-arrangement of unconsolidated, granular sediments. Liquefaction is dependent on the physical properties of the sediments and cause surface cracks, landslide, and the formation of soft-sediment deformation structures(SSDS). SSDS is formed by the combined action of the driving force and deformation mechanism(liquefaction, thixotropy, and fluidization) that is triggered by endogenic or exogenic triggers. So research on the SSDS can unravel syndepositional geological events. If detailed sedimentologic analysis together with surrounding geological context suggest SSDS formed by earthquakes, the SSDS provide a clue to unravel syndepositional tectonic activities and detailed paleoseismological information(> Mw 5) including earthquakes that leave no surface expression.

• Development and Reproduction
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• v.24 no.4
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• pp.297-306
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• 2020

Repetitive changes in the intracellular calcium concentration ([Ca²⁺]i) triggers egg activation, including cortical granule exocytosis, resumption of second meiosis, block to polyspermy, and initiating embryonic development. [Ca²⁺]i oscillations that continue for several hours, are required for the early events of egg activation and possibly connected to further development to the blastocyst stage. The sources of Ca²⁺ ion elevation during [Ca²⁺]i oscillations are Ca²⁺ release from endoplasmic reticulum through inositol 1,4,5 tri-phosphate receptor and Ca²⁺ ion influx through Ca²⁺ channel on the plasma membrane. Ca²⁺ channels have been characterized into voltage-dependent Ca²⁺ channels (VDCCs), ligand-gated Ca²⁺ channel, and leak-channel. VDCCs expressed on muscle cell or neuron is specified into L, T, N, P, Q, and R type VDCs by their activation threshold or their sensitivity to peptide toxins isolated from cone snails and spiders. The present study was aimed to investigate the localization pattern of N and P/Q type voltage-dependent calcium channels in mouse eggs and the role in fertilization. [Ca²⁺]i oscillation was observed in a Ca²⁺ contained medium with sperm factor or adenophostin A injection but disappeared in Ca²⁺ free medium. Ca²⁺ influx was decreased by Lat A. N-VDCC specific inhibitor, ω-Conotoxin CVIIA induced abnormal [Ca²⁺]i oscillation profiles in SrCl₂ treatment. N or P/Q type VDC were distributed on the plasma membrane in cortical cluster form, not in the cytoplasm. Ca²⁺ influx is essential for [Ca²⁺]i oscillation during mammalian fertilization. This Ca²⁺ influx might be controlled through the N or P/Q type VDCCs. Abnormal VDCCs expression of eggs could be tested in fertilization failure or low fertilization eggs in subfertility women.

• The Bulletin of The Korean Astronomical Society
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• v.43 no.2
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• pp.42.2-43
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• 2018

When galaxy clusters interact, the intergalactic gas collides, forming shocks that are characterized by a low sonic Mach number (~3) but a comparatively high Alfvenic Mach number (~30). Such shocks behave differently from the more common astrophysical shocks, which tend to have higher sonic Mach numbers. We wish to determine whether these shocks, despite their low sonic Mach number, are capable of accelerating particles and thereby contributing to the cosmic ray spectrum. Using the PIC-MHD method, which separates the gas into a thermal and a non-thermal component to increase computational efficiency, and relying on existing PIC simulations to determine the rate at which non-thermal particles are injected in the shock, we investigate the evolution of galaxy cluster shocks and their ability to accelerate particles. Depending on the chosen injection fraction of non-thermal particles into the shock, we find that even low-Mach shocks are capable of accelerating particles. However, the interaction between supra-thermal particles and the local magnetic field triggers instabilities and turbulence in the magnetic field. This causes the shock to weaken, which in turn reduces the effectiveness of the supra-thermal particle injection. We investigate how this influences the shock evolution by reducing the particle injection rate and energy and find that a reduction of the particle injection fraction at this stage causes an immediate reduction of both upstream and downstream instabilities. This inhibits particle acceleration. Over time, as the instabilities fade, the shock surface straightens, allowing the shock to recover. Eventually, we would expect this to increase the efficiency of the particle injection and acceleration to previous levels, starting the same series of events in an ongoing cycle of increasing and decreasing particle acceleration.