• Journal of The Korean Association For Science Education
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• v.36 no.4
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• pp.629-641
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• 2016

Understanding of how teachers change instruction can help predict what kind of educational materials is supportive or appropriate. On the basis of this idea, we explored elementary teachers' PCK progression on specific topics of astronomy: planet size and distance in solar system. To identify the development of PCK over time, we utilized learning progression (LP) as a conceptual framework. The progression of teacher PCK can also be illustrated as the hypothetical pathway from novice to expert like LP. Eight 5th grade elementary teachers participated in this study. We observed participating teachers' astronomy classes with the same topic. In order to document topic-specific PCK of participating teachers, we developed an analytic protocol consisting of four categories: knowledge of curriculum, knowledge of teaching strategies, knowledge of assessment, and astronomical thinking practice. In addition, we monitored the changes in the four participating teachers' PCK for two years in order to validate the evidences of the PCK progression. Participating teachers in this study took some intervention by attending a four-week pre-meeting with the researchers to profile an adaptive instruction. Through this research, we profiled four and five different levels of PCK progressions in three knowledge components (curriculum, teaching strategies, student assessment) and one astronomical thinking practice (systems thinking), respectively. Participating teachers demonstrated various levels and pathways in each component of PCK. This study released the empirical evidences in fostering instructional scaffolding, which is appropriate to the level of PCK of science teachers on specific topic.

• Biomolecules & Therapeutics
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• v.15 no.4
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• pp.240-244
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• 2007

Cigarette smoking causes serious health problems in humans, especially if smoking habits are established during their adolescence. Nicotine is known to mutate DNA and interfere with apoptosis. Apoptosis is considered as a potent defense mechanism against cellular damaging agents. This study aims to investigate the effect of nicotine on the progression of apoptosis induced under ER stress conditions using four different established cell lines: HEK293, 3T3-L1, C2C12, and HepG2. When treated with nicotine, the progression of apoptosis was notably inhibited in the four cell lines according to the assays of caspase-3 activation and DNA fragmentation. In ER-stressed cells, nicotine appears to inhibit the progression of apoptosis in a concentration-dependent manner. When cells were treated with nicotine prior to ER stress, GRP94 level significantly increased compared to other ER stress markers of PDI and GRP78. This observation suggests that the inhibitory effect of nicotine may results from up-regulation of GRP94, an anti-apoptotic chaperone, under nicotine treatment. Taken together, the present study strongly implies that nicotine may inhibit apoptosis, caused by prolonged ER stress, based on promotion of GRP94 expression.

• Proceedings of the Korean Society of Toxicology Conference
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• 2006.11a
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• pp.19-24
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• 2006

Mothers against decapentaplegic homolog 4 (SMAD4) is a tumor suppressor gene associated with gastrointestinal carcinogenesis. The aim of the present study was to characterize more precisely its role in the development and progression of human gastric carcinoma. In this study, using tissue microarray analysis of 283 gastric cancers and related lesions, we found loss of SMAD4 protein expression in the cytoplasm (36/114, 32%) and in the nucleus (46/114, 40%) of gastric cancer cells. The loss of nuclear SMAD4 expression in primary tumors correlated significantly with poor survival, and was an independent prognostic marker in multivariate analysis. We also found a substantial decrease in SMAD4 expression at both the RNA and protein level in several human gastric carcinoma cell lines. To identify the genetic and/or epigenetic mechanisms of altered SMAD4 expression in gastric carcinoma, loss of heterozygosity (LOH), promoter hypermethylation, and exon mutations were examined. We found that LOH (20/70, 29%) and promoter hypermethylation (4/73, 5%) were associated with the loss of SMAD4 expression. SMAD4 protein levels wore also affected in certain gastric carcinoma cell lines following incubation with Mc132, a proteasome inhibitor. Taken together, our results indicate that the loss of SMAD4, especially loss of nuclear SMAD4 expression, is involved in gastric cancer progression. The loss of SMAD4 in gastric carcinomas is due to several mechanisms, including LOH, hypermethylation, and proteasome degradation.

• Journal of The Korean Society of Emergency Medicine
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• v.29 no.6
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• pp.656-662
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• 2018

Objective: Acute appendicitis is one of the most urgent surgical problems. Several factors have been considered as predictors of perforation, but this study focused on the change in pain pattern. The degree of pain and progression of appendicitis were analyzed assuming that the pain intensity would increase until the perforation and the degree of pain would decrease immediately after the perforation occurred. Methods: In this study, 385 out of 467 patients, who were diagnosed with appendicitis in a single institution and aged between 15 and 65 years, were reviewed retrospectively. The patients' pain scores and the diameters of appendices were analyzed along with the accompanying complications. Correlation analysis and a Student's t-test were performed. Results: In patients with complicated appendicitis, the mean numerical rating scale (NRS) was slightly higher than that of simple appendicitis, but there was no significant difference in the absolute value. Only the size of the appendix showed meaningful differences according to the combined computed tomography findings. The NRS distribution or appendiceal size did not correlate with the time duration from symptom onset. Conclusion: The appendiceal size tended to increase with progressing appendicitis. No significant correlation was observed between the patient's pain level and complications. The time duration from symptom onset did not show a relationship with the progression of appendicitis.

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.1
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• pp.245-252
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• 2014

Human METCAM/MUC18, a cell adhesion molecule (CAM) in the immunoglobulin-like gene super family, plays a dual role in the progression of several epithelium cancers; however, its role in the nasopharyngeal carcinoma (NPC) remains unclear. To initiate the study we determined human METCAM/MUC18 expression in tissue samples of normal nasopharynx (NP), NPCs, and metastatic lesions, and in two established NPC cell lines. Immunoblotting analysis was used for the determination in lysates of frozen tissues, and immunohistochemistry (IHC) for expression in formalin-fixed, paraffin-embedded tissue sections of 7 normal nasopharynx specimens, 94 NPC tissue specimens, and 3 metastatic lesions. Human METCAM/MUC18 was expressed in 100% of the normal NP, not expressed in 73% of NPC specimens (or expressed at very low levels in only about 27% of NPC specimens), and expressed again in all of the metastatic lesions. The level of human METCAM/MUC18 expression in NPC tissues was about one fifth of that in the normal NP and metastatic lesions. The low level of human METCAM/MUC18 expression in NPC specimens was confirmed by a weak signal of RT-PCR amplification of the mRNA. Low expression levels of human METCAM/MUC18 in NPC tissues were also reflected in the seven established NPC cell lines. These findings provided the first evidence that diminished expression of human METCAM/MUC18 is an indicator for the emergence of NPC, but increased expression then occurs with metastatic progression, suggesting that huMETCAM/MUC18, perhaps similar to TGF-${\beta}$, may be a tumor suppressor, but a metastasis promoter for NPC.

• Safety and Health at Work
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• v.1 no.1
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• pp.69-79
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• 2010

Objectives: Various cytokines induced by inhalation of coal dust may mediate inflammation and lead to tissue damage or fibrosis, such as coal workers' pneumoconiosis (CWP). Methods: To investigate the relevance of serum cytokines in CWP, the levels of serum interleukin-8 (IL-8) and tumor necrosis factor-alpha (TNF-${\alpha}$) as CWP biomarkers in 110 retired coal miners (22 controls and 88 CWP subjects) were related to cross sectional findings and 1-year progressive changes of the pneumoconiosis. Progressive changes of CWP were evaluated by paired comparison of chest radiographs. Analysis by a receiver operating characteristic curve assessed the biomarker potential of each cytokine. Results: The mean serum IL-8 level was significantly higher in CWP compared to controls and IL-8 levels correlated with the degree of CWP. The median serum TNF-${\alpha}$ level was significantly higher in subjects with progressive CWP compared to subjects without CWP progression. The area under the ROC curve for IL-8 (0.70) and TNF-${\alpha}$ (0.72) for CWP identification and progression, respectively, indicated the biomarker potential of the two cytokines. Serum cutoff values of IL-8 and TNF-${\alpha}$ were 11.63 pg/mL(sensitivity, 69%; specificity, 64%) and 4.52 pg/mL (sensitivity, 67%; specificity, 79%), respectively. Conclusion: The results suggest that high levels of serum IL-8 are associated with the presence of CWP and those of serum TNF-${\alpha}$ are associated with the progression of CWP.

• Journal of Ginseng Research
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• v.46 no.3
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• pp.481-488
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• 2022

Background: Although the tumor-suppressive effects of ginsenosides in cell cycle have been well established, their pharmacological properties in mitosis have not been clarified yet. The chromosomal instability resulting from dysregulated mitotic processes is usually increased in cancer. In this study, we aimed to investigate the anticancer effects of ginsenoside Rg1 on mitotic progression in cancer. Materials and methods: Cancer cells were treated with ginsenoside Rg1 and their morphology and intensity of different protein were analyzed using immunofluorescence microscopy. The level of proteins in chromosomes was compared through chromosomal fractionation and Western blot analyses. The location and intensity of proteins in the chromosome were confirmed through immunostaining of mitotic chromosome after spreading. The colony formation assays were conducted using various cancer cell lines. Results: Ginsenoside Rg1 reduced cancer cell proliferation in some cancers through inducing mitotic arrest. Mechanistically, it inhibits the phosphorylation of histone H3 Thr3 (H3T3ph) mediated by Haspin kinase and concomitant recruitment of chromosomal passenger complex (CPC) to the centromere. Depletion of Aurora B at the centromere led to abnormal centromere integrity and spindle dynamics, thereby causing mitotic defects, such as increase in the width of the metaphase plate and spindle instability, resulting in delayed mitotic progression and cancer cell proliferation. Conclusion: Ginsenoside Rg1 reduces the level of Aurora B at the centromere via perturbing Haspin kinase activity and concurrent H3T3ph. Therefore, ginsenoside Rg1 suppresses cancer cell proliferation through impeding mitotic processes, such as chromosome alignment and spindle dynamics, upon depletion of Aurora B from the centromere.

• The Journal of the Korean life insurance medical association
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• v.30 no.2
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• pp.16-19
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• 2011

In patents with diabetes, the higher the serum glucose level was, the more cardiovascular events and death were observed. But with a certain kind of group, to control glucose level tightly does not decrease the incidence of these events. Several studies show that intensive glucose control does not gain benefit in patient with long standing, uncontrolled diabetes, especially having previous cardiovascular events, while definitely preventing progression of newly onset of diabetic nephropathy. Whether intensive glucose control increases mortality in high risk group is obscure and needs more studies with longer observation time.

• Interdisciplinary Bio Central
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• v.3 no.1
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• pp.5.1-5.5
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• 2011

Introduction: Many signal transduction pathways mediate cell's behavior by regulating expression level of involved genes. Abnormal behavior indicates loss of regulatory potential of pathways, and this can be attributed to loss of expression regulation of downstream genes. Therefore, function of pathways should be assessed by activity of a pathway itself and relative activity between a pathway and downstream genes, simultaneously. Results and Discussion: In this study, we suggested a new method to assess pathway's function by introducing concept of 'responsiveness'. The responsiveness was defined as a relative activity between a pathway itself and its downstream genes. The expression level of a downstream gene as a function of an upstream pathway activation characterizes disease status. In this aspect, by using the responsiveness we predicted potential progress in cancer development. We applied our method to predict primary and metastatic status of melanoma cancer. The result shows that the responsiveness-based approach achieves better performance than using gene or pathway information alone. The mean of ROC scores in the responsiveness-based approach was 0.90 for GSE7553 data set, increased more than 40% compared to a gene-based method. Moreover, identifying the abnormal regulatory patterns between pathway and its downstream genes provided more biologically interpretable information compared to gene or pathway based approaches.

• Asian Pacific Journal of Cancer Prevention
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• v.13 no.4
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• pp.1231-1233
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• 2012

Objective: The aim of this study was to explore the expression of DLC-l in breast carcinoma and any association with tumor metastasis. Methods: 51 surgical specimens of human breast carcinoma, divided into high invasive and low invasive groups according to their clinicopathological features, 30 cases of adjacent normal tissue and 28 benign breast lesions were examined by qRT-PCR for expression of DLC-1. Results: Expression level of DLC-1 in adjacent normal tissue and benign breast lesion specimens was higher than that in breast carcinoma (P<0.0001); the values in the high invasive group with synchronous metastases were also lower than in the low invasive group (P=0.0275). The correlation between DLC-1 expression level and tumor progression and metastasis of breast cancer was negative. Conclusion: As an anti-oncogene, DLC-1 could play an important part in breast carcinoma occurrence, progression, invasiveness and metastasis. Detecting the changes of the expression of DLC-1 in the breast carcinoma may contribute to earlier auxiliary diagnosis of invasiveness, metastasis and recrudescence.