• Title/Summary/Keyword: Snail trail

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Non-destructive Analysis of Snail Trail on Silver Grid Line in PV Module (비파괴 분석법을 적용한 결정질 태양전지 모듈의 Snail trail 현상 연구)

  • Kim, Dajung;Kim, Namsu;Hwang, Kyung-Jun;Lee, Ju Ho;Jeong, Sinyoung;Jeong, Dae Hong
    • Current Photovoltaic Research
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    • v.2 no.2
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    • pp.63-68
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    • 2014
  • In recent years, discoloration defects, called as snail trail, have been observed at many crystalline photovoltaic modules after a period of time ranging from several months to several years after initial installation. It has been reported that this phenomenon doesn't impact on the performance of photovoltaic modules, but it can be detected through simple visual inspection. The origin and detailed mechanism for the formation have not been identified. In this study, non-destructive analysis by Raman spectroscopy has been carried out to investigate the origin of this phenomenon. In parallel, destructive analysis by scanning electron microscopt and transmission electron microscopy was also performed in order to confirm the results from non-destructive method. Through the extensive analysis, it was found that the main cause for discoloration is the formations of $Ag_2CO_3$ and $AgC_2H_3O_2$. Detailed mechanism for the formation of these particles was indentified through systematic studies.

Extracellular acidity enhances tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-mediated apoptosis via DR5 in gastric cancer cells

  • Hong, Ran;Han, Song Iy
    • The Korean Journal of Physiology and Pharmacology
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    • v.22 no.5
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    • pp.513-523
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    • 2018
  • The tumor microenvironment greatly influences cancer cell characteristics, and acidic extracellular pH has been implicated as an essential factor in tumor malignancy and the induction of drug resistance. Here, we examined the characteristics of gastric carcinoma (GC) cells under conditions of extracellular acidity and attempted to identify a means of enhancing treatment efficacy. Acidic conditions caused several changes in GC cells adversely affecting chemotherapeutic treatment. Extracellular acidity did inhibit GC cell growth by inducing cell cycle arrest, but did not induce cell death at pH values down to 6.2, which was consistent with down-regulated cyclin D1 and up-regulated p21 mRNA expression. Additionally, an acidic environment altered the expression of atg5, HSPA1B, collagen XIII, collagen XXAI, slug, snail, and zeb1 genes which are related to regulation of cell resistance to cytotoxicity and malignancy, and as expected, resulted in increased resistance of cells to multiple chemotherapeutic drugs including etoposide, doxorubicin, daunorubicin, cisplatin, oxaliplatin and 5-FU. Interestingly, however, acidic environment dramatically sensitized GC cells to apoptosis induced by tumor necrosis factor-related apoptosis-inducing ligand (TRAIL). Consistently, the acidity at pH 6.5 increased mRNA levels of DR4 and DR5 genes, and also elevated protein expression of both death receptors as detected by immunoblotting. Gene silencing analysis showed that of these two receptors, the major role in this effect was played by DR5. Therefore, these results suggest that extracellular acidity can sensitize TRAIL-mediated apoptosis at least partially via DR5 in GCs while it confers resistance to various type of chemotherapeutic drugs.