Climate Change Impact Assessment on Han River Long Term Runoff in South Korea Based on RCP Climate Change Scenario

The 2007 World Economic Forum (WEF) referred to climate change as the overriding problem we face. Concerns have been raised about how global warming would accelerate future climate change and its consequences. Many climate change studies expect the possible occurrence of extreme high temperature, increase in heavy rains and strong typhoons in the near future. Currently, climate change scenarios are used to prepare an appropriate plan for these phenomena under climate change. The main purpose of this paper is to suggest and evaluate an operational method of assessing the potential impact of climate change on hydrologic components and water resources at the regional scale. Future runoff was simulated using high resolution Regional Circulation Model (RCM) (12.5 × 12.5 km) Representative Concentration Pathway (RCP) scenario operated by the Korea Meteorological Administration (KMA) and a semi-distribution model or SLURP (Semi-distributed Land Use-based Runoff Process). The study was carried out on the Han River including its nine dams. The study found that runoff characteristics, especially annual distribution, could change. The discharge in July tends to decrease while runoff can increase in August and September. The flow duration curve was estimated and compared with observed data and simulated daily runoff data for Paldang-dam to evaluate the effect of climate change. The analysis of the flow duration curve shows that the mean average low flow increased while the average wet and normal flow decreased under the climate change scenario

A review of current studies on cellular and molecular mechanisms underlying pulmonary fibrosis induced by chemicals

Several studies showed that the inflammatory and fibrotic responses induced by polyhexamethylene guanidine phosphate (PHMG-p) were similar to those observed for idiopathic pulmonary fibrosis in South Korea in 2011. “Omic” technologies can be used to understand the mechanisms underlying chemical-induced diseases. Studies to determine the toxicity of chemicals may facilitate understanding of the mechanisms underlying the development of pulmonary fibrosis at a molecular level; thus, such studies may provide information about the toxic characteristics of various substances. In this review, we have outlined the cellular and molecular mechanisms underlying idiopathic pulmonary fibrosis and described pulmonary fibrosis induced by various chemicals, including bleomycin, paraquat, and PHMG-p, based on the results of studies performed to date

Fibrinogen gamma-A chain precursor in CSF: a candidate biomarker for Alzheimer's disease

<p>Abstract</p> <p>Background</p> <p>Cerebrospinal fluid (CSF) may be valuable for exploring protein markers for the diagnosis of Alzheimer's disease (AD). The prospect of early detection and treatment, to slow progression, holds hope for aging populations with increased average lifespan. The aim of the present study was to investigate candidate CSF biological markers in patients with mild cognitive impairment (MCI) and AD and compare them with age-matched normal control subjects.</p> <p>Methods</p> <p>We applied proteomics approaches to analyze CSF samples derived from 27 patients with AD, 3 subjects with MCI and 30 controls. The AD group was subdivided into three groups by clinical severity according to clinical dementia rating (CDR), a well known clinical scale for dementia.</p> <p>Results</p> <p>We demonstrated an elevated level of fibrinogen gamma-A chain precursor protein in CSF from patients with mild cognitive impairment and AD compared to the age-matched normal subjects. Moreover, its expression was more prominent in the AD group than in the MCI and correlated with disease severity and progression. In contrast, fibrinogen gamma-A chain precursor protein was detected very low in the age-matched normal group.</p> <p>Conclusion</p> <p>These findings suggest that the CSF level of fibrinogen gamma-A chain precursor may be a candidate biomarker for AD.</p

Improving shear bond strength of temporary crown and fixed dental prosthesis resins by surface treatments

This article is published with open access at Springerlink.comThis study evaluated the effect of surface treatments on the bond strength of repaired temporary resins. One-hundred flat-surfaced cylindrical specimens (Ø 7 mm × 12 mm) of each temporary resin (2 bis-acryl resins and 2 polymethyl-methacrylates) were prepared. The specimens were randomly divided into 10 groups (n = 10), according to the types of surface treatments: untreated, adhesive treated, silanated, silane + adhesive treated, hydrofluoric acid etched, laser treated, sandblasted, sandblasting + adhesive treated, sandblasting + silanated, and tribochemical silica coating + silanated. Each resin material of the same brand with cylindrical shape (Ø 3 mm × 3 mm) was polymerized onto the resin surfaces, and specimens were stored for 24 h in distilled water. The shear bond strengths were measured and failure modes were examined. All data were analyzed with a one-way ANOVA and multiple comparison Scheffé post hoc test (α = 0.05). For bis-acryl resins, the highest shear bond strength was observed in sandblasted group and the lowest was observed in the control group. Results show that the repair bond strength was improved for bis-acryl resin by 23 % than that of the control group due to the increase in surface roughness by sandblasting. However, chemical treatment did not improve repair bond strength. The surface treatment of bis-acryl resins with sandblasting seems to be promising for the improvement of repair bond strength.OAIID:oai:osos.snu.ac.kr:snu2015-01/102/2008003883/12ADJUST_YN:NEMP_ID:A078517DEPT_CD:861CITE_RATE:2.371FILENAME:j mater sci 201510 51(3) 1463-75.pdfDEPT_NM:치의학과SCOPUS_YN:YCONFIRM:

The overexpression of TDP-43 in astrocytes causes neurodegeneration via a PTP1B-mediated inflammatory response

Background: Cytoplasmic inclusions of transactive response DNA binding protein of 43 kDa (TDP-43) in neurons and astrocytes are a feature of some neurodegenerative diseases, such as frontotemporal lobar degeneration with TDP-43 (FTLD-TDP) and amyotrophic lateral sclerosis (ALS). However, the role of TDP-43 in astrocyte pathology remains largely unknown. Methods: To investigate whether TDP-43 overexpression in primary astrocytes could induce inflammation, we transfected primary astrocytes with plasmids encoding Gfp or TDP-43-Gfp. The inflammatory response and upregulation of PTP1B in transfected cells were examined using quantitative RT-PCR and immunoblot analysis. Neurotoxicity was analysed in a transwell coculture system of primary cortical neurons with astrocytes and cultured neurons treated with astrocyte-conditioned medium (ACM). We also examined the lifespan, performed climbing assays and analysed immunohistochemical data in pan-glial TDP-43-expressing flies in the presence or absence of a Ptp61f RNAi transgene. Results: PTP1B inhibition suppressed TDP-43-induced secretion of inflammatory cytokines (interleukin 1 beta (IL-1β), interleukin 6 (IL-6) and tumour necrosis factor alpha (TNF-α)) in primary astrocytes. Using a neuron-astrocyte coculture system and astrocyte-conditioned media treatment, we demonstrated that PTP1B inhibition attenuated neuronal death and mitochondrial dysfunction caused by overexpression of TDP-43 in astrocytes. In addition, neuromuscular junction (NMJ) defects, a shortened lifespan, inflammation and climbing defects caused by pan-glial overexpression of TDP-43 were significantly rescued by downregulation of ptp61f (the Drosophila homologue of PTP1B) in flies. Conclusions: These results indicate that PTP1B inhibition mitigates the neuronal toxicity caused by TDP-43-induced inflammation in mammalian astrocytes and Drosophila glial cells. © 2020, The Author(s).1