• Journal of Digital Convergence
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• v.13 no.10
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• pp.107-120
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• 2015

In this paper, we study the conflict management plan of the organization in the age of convergence. More specifically, we reveal the impact of the conflict according to behavior of the leader. To this purpose, The behavior of the leader were classified as Supportive Leader and Controlled Leader, and forms of Resistance wert classified as Functional Resistance and Dysfunctional Resistance that results of the conflict. Also, Psychological Contract Violation and Breach was set up as a mediate variable. The results were as follows. First, When employee resistance comes up in the organization, Support behavior of Leaders leads to desirable changes in the organization through the functional and constructive resistance. In contrast, Controlled behavior of Leaders leads the destructive and dysfunctional resistance of employee. Second, Since the perception that the follower is receiving assistance to leaders, it reduces the perception of psychological contract violation, but Controlled leader is largely perceived as the Psychological Contract Violation to the followers. Third, Supportive Leader is not influence the affect of employee, and They resolve the Conflict in objective and positive way. Therefore, the results of this study have many theoretical and practical implications.

• Toxicological Research
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• v.30 no.3
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• pp.141-148
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• 2014

Endothelium-derived relaxing factors (EDRFs), including nitric oxide (NO), prostacyclin ($PGI_2$), and endothelium-derived hyperpolarizing factor (EDHF), play pivotal roles in regulating vascular tone. Reduced EDRFs cause impaired endothelium-dependent vasorelaxation, or endothelial dysfunction. Impaired endothelium-dependent vasorelaxation in response to acetylcholine (ACh) is consistently observed in conduit vessels in human patients and experimental animal models of hypertension. Because small resistance arteries are known to produce more than one type of EDRF, the mechanism(s) mediating endothelium-dependent vasorelaxation in small resistance arteries may be different from that observed in conduit vessels under hypertensive conditions, where vasorelaxation is mainly dependent on NO. EDHF has been described as one of the principal mediators of endothelium-dependent vasorelaxation in small resistance arteries in normotensive animals. Furthermore, EDHF appears to become the predominant endothelium-dependent vasorelaxation pathway when the endothelial NO synthase (NOS3)/NO pathway is absent, as in NOS3-knockout mice, whereas some studies have shown that the EDHF pathway is dysfunctional in experimental models of hypertension. This article reviews our current knowledge regarding EDRFs in small arteries under normotensive and hypertensive conditions.

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.24
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• pp.10847-10853
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• 2015

Background: Lapatinib, a dual tyrosine kinase inhibitor that interrupts the epidermal growth factor receptor (EGFR) and HER2/neu pathways, has been indicated to have significant efficacy in treating HER2-positive breast cancer. However, acquired drug resistance has become a very serious clinical problem that hampers the use of this agent. In this study, we aimed to screen small molecule drugs that might reverse lapatinib-resistance of breast cancer by exploring differentially expressed genes (DEGs) via a bioinformatics method. Materials and Methods: We downloaded the gene expression profile of BT474-J4 (acquired lapatinib-resistant) and BT474 (lapatinib-sensitive) cell lines from the Gene Expression Omnibus (GEO) database and selected differentially expressed genes (DEGs) using dChip software. Then, gene ontology and pathway enrichment analyses were performed with the DAVID database. Finally, a connectivity map was utilized for predicting potential chemicals that reverse lapatinib-resistance. Results: A total of 1, 657 DEGs were obtained. These DEGs were enriched in 10 pathways, including cell cycling, regulation of actin cytoskeleton and focal adhesion associate examples. In addition, several small molecules were screened as the potential therapeutic agents capable of overcoming lapatinib-resistance. Conclusions: The results of our analysis provided a novel strategy for investigating the mechanism of lapatinib-resistance and identifying potential small molecule drugs for breast cancer treatment.

• Journal of Families and Better Life
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• v.31 no.5
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• pp.47-63
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• 2013

This study deals with a counseling case in which a mother requested counseling due to the problems of her daughter, who suffers from multiple tic disorder. The participants of this study included five family members (grandmother, father, mother and two female children) and a total of 23 sessions were held from September 2006 to December 2007. Additional counseling ($24^{th}$ counseling session) was conducted on April 1st, 2009. The data was based on recorded transcripts and notes from 24 family therapy sessions. The study used a constant comparative analysis, which uses matrix and network display as an analysis method suggested by Miles&Huberman(1994). The characteristics of the family of origin and the indifference of the husband had caused the wife stress. The couple had frequent conflicts due to dysfunctional communication methods, a clash of values, sexual dissatisfaction, and a lack of communication. This marital conflict became the primary factor of the daughter's multiple tic disorder. Intervention of the family therapist resulted in the setting of treatment goals based on MRI's communication theory and Bowen's family systems theory in order to solve the problem of the daughter's multiple tic disorder. Also, the therapist's intervention techniques included exploring experiences with the family of origin, shedding light on the multigenerational transmission process, exploring dysfunctional attempts at solutions, the therapist's self-disclosure, providing similar cases, dealing with resistance, and suggesting a new communication method. To solve the problem, the therapist helped the family separate the daughter spatially from her parents. Therefore, the therapist's intervention helped reduce the daughter's tics and improve relationships among the family.

• Journal of Life Science
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• v.29 no.9
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• pp.1034-1046
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• 2019

The mitochondria is the major cellular organelle of energy metabolism for the supply of cellular energy; it also plays an important role in controlling calcium regulation, reactive oxygen species (ROS) production, and apoptosis. Mitochondrial dysfunction causes various diseases, such as neurodegenerative diseases, Lou Gehrig's disease, cardiovascular disease, mental disorders, diabetes, and cancer. Most of the diseases are age-related diseases. In this review, we focus on the roles of mitochondrial dysfunction in cancer. Mitochondrial dysfunction induces carcinogenesis and is found in many cancers. The factors that cause mitochondrial dysfunction differ depending on the types of carcinoma, and those factors could cause cancer malignancy, such as resistance to therapy and metastasis. Mitochondrial dysfunction is caused by a lack of mitochondria, an inability to provide key substances, or a dysfunction in the ATP synthesis machinery. The main factor associated with cancer malignancy is mtDNA depletion. Mitochondrial dysfunction would leads to malignancy through changes in molecular activity or expression, but it is not known in detail which changes lead to cancer malignancy. In order to explore the relationship between mitochondrial dysfunction and cancer malignancy in detail, mitochondria dysfunctional cell lines are constructed using chemical methods such as EtBr treatment or gene editing methods, including shRNA and CRISPR/Cas9. Those mitochondria dysfunctional cell lines are used in the study of various diseases caused by mitochondrial dysfunction, including cancer.

• Childhood Kidney Diseases
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• v.3 no.2
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• pp.209-216
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• 1999

Purpose : Nephrogenic diabetes insipidus (NDI) is a rare X-linked disorder associated with renal tubule resistance to arginine vasopressin (AVP). The hypothesis that the defect underlying NDI might be a dysfunctional renal AVPR2 has recently been proven by the identification of mutations in the AVPR2 gene in NDT patients. To investigate the association of mutations in th AVPR2 gene with NDI, we analyzed the AVPR2 gene located on the X chromosome. Methods : We have analyzed the AVPR2 gene in a kindred with X-linked NDI. The proband and proband's mother were analyzed by polymerase chain reaction-single strand conformational polymorphism(PCR-SSCP) and DNA sequencing of the AVPR2 gene. We also have used restriction enzyme analysis of genomic PCR product to evaluate the AVPR2 gene. Results : C to T transition at codon 202, predictive of an exchange of tryptophan 202 by cysteine(R202C) in the third extracellular domain was identified. This mutation causes a loss of Hae III site within the gene. Conclusion : We found a R202C missense mutation in the AVPR2 gene causing X-linked NDI, and now direct mutational analysis is available for carrier screening and early diagnosis.