• Tuberculosis and Respiratory Diseases
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• v.46 no.2
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• pp.185-194
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• 1999

Background: NF-$\kappa$B is a characteristic transcriptional factor whose functional activity is determined by post-translational modification of protein and subsequent change of subcellular localization. The involvement of the NF-$\kappa$B family of the transcription factors in the control of such vital cellular functions as immune response, acute phase reaction, replication of certain viruses and development and differentiation of cells has been clearly documented in many previous studies. Several recent observations have suggested that the NF-$\kappa$B might also be involved in the carcinogenesis of some hematological and solid tumors. Investigating the possibility that members of the NF-$\kappa$B family participate in the molecular control of malignant cell transformation could provide invaluable information on both molecular pathogenesis and cancer-related gene therapy. Method: To determine the expression patterns and functional roles of NF-$\kappa$B family transcription factors in human lung cancer cell lines NCI-H792, NCI-H709, NCI-H226 and NCI-H157 were analysed by western blot, using their respective antibodies. The nuclear and the cytoplasmic fraction of protein extract of these cell lines were subsequently obtained and NF-$\kappa$B expression in each fraction was again determined by western blot analysis. The type of NF-$\kappa$B complex present in the cells was determined by immunoprecipitation. To detect the binding ability of cell-line nuclear extracts to the KB consensus oligonucleotide, electrophoretic mobility shift assay(EMSA) was performed. Results: In the cultured human lung cancer cell lines tested, transcription factors of the NF-$\kappa$B family, namely the p50 and p65 subunit were expressed and localized in the nuclear fraction of the cellular extract by western blot analysis and immunocytochemistry. Immunoprecipitation assay showed that in the cell, the p50 and p65 subunits made NF-$\kappa$B complex. Finally it was shown by Electrophoretic Mobility Shift Assay(EMSA) that nuclear extracts of lung cancer cell lines are able to bind to NF-$\kappa$B consensus DNA sequences. Conclusion: These data suggest that in human lung cancer cell lines the NF-$\kappa$B p50/p65 complex might be activated. and strengthen the hypothesis that NF-$\kappa$B family transcription factors might be involved in the carcinogenesis of human lung cancer.

• Korean Journal of Psychosomatic Medicine
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• v.4 no.2
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• pp.269-276
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• 1996

A theroretical study was made on the psychodynamism of somatoform disorder. Somatoform disorder is caused by a defense mechanism of somatization. Somatization is the tendency to react to stimuli(drives, defenses, and conflict between them) physically rather than psychically(Moore, 1990). Ford(1983) said it is a way of life, and Dunbar(1954) said it is the shift of psychic energy toward expression in somatic symptoms. As used by Max Shur(1955), somatization links symptom formation to the regression that may occur in response to acute and chronic conflict. In the neurotic individual psychic conflict often provokes regressive phenomena that may include somatic manifestations characteristic of an earlier developmental phase. Schur calls this resomatization. Pain is the most common example of a somatization reaction to conflict. The pain has an unconscious significance derived from childhood experiences. It is used to win love, to punish misdeeds, as well as a means to amend. Among all pains, chest pain has a special meaning. Generally speaking, 'I have pain in my chest' is about the same as 'I have pain in my mind'. The chest represent the mind, and the mind reminds us about the heart. So we have a high tendency to recognize mental pain as cardiac pain. Kellner(1990) said rage and hostility, especially repressed hostility, are important factors in somatization. In 'Psychoanalytic Observation on Cardiac Pain', psychoanalyst Bacon(1953) presented clinical cases of patients who complained of cardiac pain in a psychoanalytic session that spread from the left side of their chests down their left arms. The pain was from rage and fear which came after their desire to be loved was frustrated by the analyet. She said desires related to cardiac pain were dependency needs and aggressions. Empatic relationship and therapeutic alliances are indispensable to psychotherapy in somatoform disorder. The beginning of therapy is to discover a precipitating event from the time their symptoms have started and to help the patient understand a relation between the symptom and precipitating event. Its remedial process is to find and interpret a intrapsychic conflict shown through the symptoms of the patient. Three cases of somatoform disorder patients treated based on this therapeutic method were introduced. The firt patient, Mr. H, had been suffering from hysterical aphasia with repressed rage as ie psychodynamic cause. An interpretation related to the precipitating event was given by written communication, and he recovered from his aphasia after 3 days of the session. The second patient was a dentist in a cardiac neurosis with agitation and hypochondriasis, whose psychodynamism was caused by a fear that he might lose his father's love. His symptom was also interpreted in relation to the precipitating event. It showed the patient a child-within afraid of losing his father's love. His condition improved after getting a didactic interpretation which told him, to be master of himself, The third patient was a lady transferred from the deparment of internal medicine. She had a frequent and violent fit of chest pains, whose psychodynamic cause was separation anxiety and a rage due to the frustration of dependency needs. Her symptom vanished dramatically when she wore a holler EKG monitor and did not occur during monitoring. By this experience she found her symptom was a psychogenic one, and a therapeutic alliance was formed. later in reguar psychotherapy sessions, she was told the relaton between symptoms and precipitating events. Through this she understood that her separation anxiety was connected to the symptom and she became less terrifide when it occurred. Now she can travel abroad and take well part in social activities.

• Tuberculosis and Respiratory Diseases
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• v.52 no.5
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• pp.485-496
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• 2002

Background : The NF-${\kappa}B$ transcription factors control various biological processes including the immune response, acute phase reaction and cell cycle regulation. NF-${\kappa}B$ complexes are retained in the cytoplasm in the basal state and various stimuli cause a translocation of the NF-${\kappa}B$ complexes into the nucleus where they bind to the ${\kappa}B$ elements and regulate the transcription of the target genes. Recent reports also suggest that NF-${\kappa}B$ proteins are involved in oncogenesis, tumor growth and metastasis. High expression of NF-${\kappa}B$ expression was reported in many cancer cell lines and tissues. The constitutive activation of NF-${\kappa}B$ was also reported in several cancer cell lines supporting its role in cancer development and survival. The anti-apoptotic action of NF-${\kappa}B$ is important for cancer survival. NF-${\kappa}B$ also controls the expression of several proteins that are important for cellular adhesion (ICAM-1, VCAM-1) suggesting a role in cancer metastasis. In lung cancer, high expression levels of the NF-${\kappa}B$ subunit p50 and c-Rel were reported. In fact, high expression does not mean a high activity, and the activation pattern of NF-${\kappa}B$ in lung cancer has not been reported. Materials and Methods : In this study, the NF-${\kappa}B$ nuclear binding activity in the basal and TNF-${\alpha}$ stimulated states were exmined in various lung cancer cell lines and compared with the normal bronchial epithelial cell line. Twelve lung cancer cell lines including the non-small cell and small cell lung cancer cell lines (A549, NCI-H358, NCI-H441, NCI-H552, NCI-H2009, NCI-H460, NCI-H1229, NCI-H1703, NCI-H157, NCI-H187, NCI-H417, NCI-H526) and BEAS-2B bronchial epithelial cell line were used. To evaluate the NF-${\kappa}B$ expression and DNA binding activity, western blot analysis and an electrophoretic mobility shift assay with the nuclear protein extracts. Results : The basal expressions of the p65 and p50 subunits were observed in the BEAS-2B cell line and all lung cancer cell lines except for NCI-H358 and NCI-H460. The expression levels of p65 and p50 were increased 30 minutes after stimulation with TNF-${\alpha}$ in BEAS-2B and in 10 lung cancer cell lines. In the NCI-H358 and NCI-H460 cell lines, p65 expression was not observed in the basal and stimulated states and the two p50 related protein levels were higher after stimulation with TNF-${\alpha}$ These new proteins were smaller than p50 and are thought to be variants of p50. In the basal state, NF-${\kappa}B$ was nearly activated in the BEAS-2B and all lung cancer cell lines. The DNA binding activity of the NF-${\kappa}B$ complexes was markedly higher after stimulation with TNF-${\alpha}$ In the BEAS-2B and all lung cancer cell line except for NCI-H358 and NCI-H460, the activated NF-${\kappa}B$ complex was a p65/p50 heterodimer. In the NCI-H358 and NCI-H460 lung cancer cell lines, the NF-${\kappa}B$ complex was variant of a p50/p50 homodimer. Conclusion : The NF-${\kappa}B$ activation pattern in the lung cancer cell lines and the normal bronchial epithelial cell lines was similar except for the activation of a variant of the p50/p50 homodimer in some lung cancer cell linse.