• The Journal of the Korea Contents Association
• /
• v.22 no.6
• /
• pp.273-282
• /
• 2022

The narrative of the film, Sweet Smell of Success has a multi-layered structure. In Clifford Odets's scenario work, numerous lines for the main plot and subplots repeated a cycle of creation, decomposition, deletion, and modification to enhance the density of the story. As a result, whenever an actor spoke a line or paused, an action or an event that would trigger another line was created, giving depth and persuasiveness to the character's performance. The music of Sweet Smell of Success has multi-layered elements. The non-diegetic music was covered by the orchestral pieces performed by Elmer Bernstein's big band orchestra and the jazz pieces performed by Fred Katz's combo band. The diegetic music was mostly covered by the jazz pieces performed by the Chico Hamilton Quintet. The practical task of the film music was to reinforce or supplement the effect of the narrative driver, and the additional task was to realize the estrangement effect and the aesthetics of stagnation. The possibility and significance of intertextuality of subplots and double sound of this film are not simply confined to the limits of the film noir genre.

• Journal of Dental Anesthesia and Pain Medicine
• /
• v.22 no.1
• /
• pp.19-27
• /
• 2022

Background: Myofascial pain dysfunction syndrome (MPDS) is the most common type of temporomandibular disorder. This study compared the efficacies of low-level diode laser therapy (LLLT) and laser acupuncture therapy (LAT) in the treatment of MPDS. Methods: This double-blind randomized controlled clinical trial included 24 patients with MPDS who were randomly divided into two equally sized groups. Patients in the LLLT group received 12 sessions of low-level diode laser irradiation applied to the trigger points of the masticatory muscles during 1 month. The same protocol was also used in the LAT group according to the specific trigger points. We measured pain intensity and maximum mouth opening in both groups at baseline, during treatment, and 2 months after treatment completion. Results: The pain intensities decreased from 6.58±1.31 to 0.33±0.65 and from 7.08 ± 1.37 to 0 in the LLLT and LAT groups, respectively. The maximum mouth openings increased from 32.25 ± 8.78 mm to 42.58 ± 4.75 mm and from 33 ± 6.57 mm to 45.67 ± 3.86 mm in the LLLT and LAT groups, respectively. Pain intensity (P = 0.839) and level of maximum mouth opening (P = 0.790) did not differ significantly between the groups. Conclusion: Our results showed similar efficacy between LLLT and LAT in the treatment of MPDS signs and symptoms.

• Journal of Microbiology and Biotechnology
• /
• v.31 no.1
• /
• pp.79-91
• /
• 2021

γ-Glutamylcysteine synthetase (Gcs1) and glutathione reductase (Glr1) activity maintains minimal levels of cellular methylglyoxal in Candida albicans. In glutathione-depleted Δgcs1, we previously saw that NAD(H)-linked methylglyoxal oxidoreductase (Mgd1) and alcohol dehydrogenase (Adh1) are the most active methylglyoxal scavengers. With methylglyoxal accumulation, disruptants lacking MGD1 or ADH1 exhibit a poor redox state. However, there is little convincing evidence for a reciprocal relationship between methylglyoxal scavenger genes-disrupted mutants and changes in glutathione-(in)dependent redox regulation. Herein, we attempt to demonstrate a functional role for methylglyoxal scavengers, modeled on a triple disruptant (Δmgd1/Δadh1/Δgcs1), to link between antioxidative enzyme activities and their metabolites in glutathione-depleted conditions. Despite seeing elevated methylglyoxal in all of the disruptants, the result saw a decrease in pyruvate content in Δmgd1/Δadh1/Δgcs1 which was not observed in double gene-disrupted strains such as Δmgd1/Δgcs1 and Δadh1/Δgcs1. Interestingly, Δmgd1/Δadh1/Δgcs1 exhibited a significantly decrease in H2O2 and superoxide which was also unobserved in Δmgd1/Δgcs1 and Δadh1/Δgcs1. The activities of the antioxidative enzymes erythroascorbate peroxidase and cytochrome c peroxidase were noticeably higher in Δmgd1/Δadh1/Δgcs1 than in the other disruptants. Meanwhile, Glr1 activity severely diminished in Δmgd1/Δadh1/Δgcs1. Monitoring complementary gene transcripts between double gene-disrupted Δmgd1/Δgcs1 and Δadh1/Δgcs1 supported the concept of an unbalanced redox state independent of the Glr1 activity for Δmgd1/Δadh1/Δgcs1. Our data demonstrate the reciprocal use of Eapx1 and Ccp1 in the absence of both methylglyoxal scavengers; that being pivotal for viability in non-filamentous budding yeast.

• Molecules and Cells
• /
• v.27 no.6
• /
• pp.689-695
• /
• 2009

Chemically synthesized small interfering RNAs (siRNAs) can specifically knock-down expression of target genes via RNA interference (RNAi) pathway. To date, the length of synthetic siRNA duplex has been strictly maintained less than 30 bp, because an early study suggested that double-stranded RNAs (dsRNAs) longer than 30 bp could not trigger specific gene silencing due to the induction of non-specific antiviral interferon responses. Contrary to the current belief, here we show that synthetic dsRNA as long as 38 bp can result in specific target gene silencing without non-specific antiviral responses. Using this longer duplex structure, we have generated dsRNAs, which can simultaneously knock-down expression of two target genes (termed as dual-target siRNAs or dsiRNAs). Our results thus demonstrate the structural flexibility of gene silencing siRNAs, and provide a starting point to construct multifunctional RNA structures. The dsiRNAs could be utilized to develop a novel therapeutic gene silencing strategy against diseases with multiple gene alternations such as viral infection and cancer.

• Journal of Genetic Medicine
• /
• v.13 no.1
• /
• pp.1-13
• /
• 2016

Although some mutations are beneficial and are the driving force behind evolution, it is important to maintain DNA integrity and stability because it contains genetic information. However, in the oxygen-rich environment we live in, the DNA molecule is under constant threat from endogenous or exogenous insults. DNA damage could trigger the DNA damage response (DDR), which involves DNA repair, the regulation of cell cycle checkpoints, and the induction of programmed cell death or senescence. Dysregulation of these physiological responses to DNA damage causes developmental defects, neurological defects, premature aging, infertility, immune system defects, and tumors in humans. Some human syndromes are characterized by unique neurological phenotypes including microcephaly, mental retardation, ataxia, neurodegeneration, and neuropathy, suggesting a direct link between genomic instability resulting from defective DDR and neuropathology. In this review, rare human genetic disorders related to abnormal DDR and damage repair with neural defects will be discussed.

• Journal of Oral Medicine and Pain
• /
• v.30 no.3
• /
• pp.345-351
• /
• 2005

The purpose of this double-blind study was to evaluate clinical effects of botulinum toxin type A (BTX-A) injection on myofascial pain syndrome (MPS) involving upper trapezius and compare with those of lidocaine injection. 21 patients presenting with active TrP1 and/or TrP2 in the upper trapezius over 6 months were selected for this study. The subjects were randomly divided into two groups; one group injected with BTX-A (15 unit of $Botox^{(R)}$ / 0.3 ml per trigger point (TrP)) and the other group injected with 0.5% lidocaine (0.3 ml /TrP). The clinical effects were evaluated by VAS and PPT at baseline, 2, 4, 6 and 8 weeks after treatment. BTX-A group showed persistent decrease of VAS values and increase of PPT values following treatment. While there was no significant difference in VAS values between BTX-A and lidocaine groups (p=0.347), there was significant difference in PPT values after treatment between two groups (p=0.000). The subjects received BTX-A showed noticeable improvement in PPT values after treatment, suggesting more reliable effect of BTX-A injection compared with lidocaine injection. The results of this study support that the direct injection of BTX-A to a TrP is an effective and safe treatment for MPS involving upper trapezius.

• Nutrition Research and Practice
• /
• v.14 no.5
• /
• pp.478-489
• /
• 2020

BACKGROUND/OBJECTIVES: Morusin, a marker component of Morus alba L., possesses anti-cancer activity. The objective of this study was to determine autophagy-inducing effect of morusin in non-small cell lung cancer (NSCLC) cells and investigate the underlying mechanism. SUBJECTS/METHODS: Autophagy induction and the expression of autophagy-related proteins were analyzed by LC3 immunofluorescence and western blot, respectively. The role of autophagy and AMP-activated protein kinase (AMPK) was determined by treating NSCLC cells with bafilomycin A1, an autophagy inhibitor, and compound C, an AMPK inhibitor. Cytotoxicity and apoptosis induction were determined by MTT assay, trypan blue exclusion assay, annexin V-propidium iodide (PI) double staining assay, and cell cycle analysis. RESULTS: Morusin increased the formation of LC3 puncta in the cytoplasm and upregulated the expression of autophagy-related 5 (Atg5), Atg12, beclin-1, and LC3II in NSCLC cells, demonstrating that morusin could induce autophagy. Treatment with bafilomycin A1 markedly reduced cell viability but increased proportions of sub-G1 phase cells and annexin V-positive cells in H460 cells. These results indicate that morusin can trigger autophagy in NSCLC cells as a defense mechanism against morusin-induced apoptosis. Furthermore, we found that AMPK and its downstream acetyl-CoA carboxylase (ACC) were phosphorylated, while mammalian target of rapamycin (mTOR) and its downstream p70S6 kinase (p70S6K) were dephosphorylated by morusin. Morusin-induced apoptosis was significantly increased by treatment with compound C in H460 cells. These results suggest that morusin-induced AMPK activation could protect NSCLC cells from apoptosis probably by inducing autophagy. CONCLUSIONS: Our findings suggest that combination treatment with morusin and autophagy inhibitor or AMPK inhibitor might enhance the clinical efficacy of morusin for NSCLC.

• Asian Pacific Journal of Cancer Prevention
• /
• v.16 no.11
• /
• pp.4543-4548
• /
• 2015

Background: To investigate the effects of ASMase mediated endothelial cell apoptosis in multiple hypofractionated irradiations in CT26 tumor bearing mice. Materials and Methods: Thirty-five CT26 tumor bearing mice were subjected to single ionizing radiation (IR) of 0, 3, 6, 9, 12, 15, 18 Gy. Eight hours after IR, the mice were sacrificed and tumor tissues were used for CD31 immunohistochemistry staining, TUNEL and CD31 double staining, ASMase activity assay. Then 6 and 12 Gy were chosen for multiple hypofractionated IR experiments according to the above results. Each time after IR, 5 mice were sacrificed and assayed as above. Results: The ASMase activities were increased significantly after a single IR of 12 Gy or higher which was accompanied with remarkable increased endothelial cell apoptosis and decreased MVD. For 6 Gy which was not high enough to trigger ASMase activation, after 2 or more times of IR, the ASMase activities were significantly increased accompanied with remarkable increased endothelial cell apoptosis and decreased MVD. While for 12 Gy, after 2 or more times of IR, the ASMase activities and endothelial cell apoptosis rates were maintained without remarkable increase; however, the MVD was significantly decreased. What's more, the cancer cell apoptosis rates were significantly increased after multiple IR for both 6 Gy and 12 Gy. Conclusions: ASMase mediated endothelial cell apoptosis may play an important role in the process of multiple hypofractionated IR for CT26 colorectal carcinoma.

• Molecules and Cells
• /
• v.42 no.12
• /
• pp.869-883
• /
• 2019

Interleukin (IL)-15 is an essential immune-modulator with high potential for use in cancer treatment. Natural IL-15 has a low biological potency because of its short half-life and difficulties in mass-production. IL-15Rα, a member of the IL-15 receptor complex, is famous for its high affinity to IL-15 and its ability to lengthen the half-life of IL-15. We have double-transfected IL-15 and its truncated receptor IL-15Rα into CT26 colon cancer cells to target them for intracellular assembly. The secreted IL-15:IL-15Rα complexes were confirmed in ELISA and Co-IP experiments. IL-15:IL-15Rα secreting clones showed a higher anti-tumor effect than IL-15 secreting clones. Furthermore, we also evaluated the vaccine and therapeutic efficacy of the whole cancer-cell vaccine using mitomycin C (MMC)-treated IL-15:IL-15Rα secreting CT26 clones. Three sets of experiments were evaluated; (1) therapeutics, (2) vaccination, and (3) long-term protection. Wild-type CT26-bearing mice treated with a single dose of MMC-inactivated secreted IL-15:IL-15Rα clones prolonged survival compared to the control group. Survival of MMC-inactivated IL-15:IL-15Rα clone-vaccinated mice (without any further adjuvant) exceeded up to 100%. This protection effect even lasted for at least three months after the immunization. Secreted IL-15:IL-15Rα clones challenging trigger anti-tumor response via CD4⁺ T, CD8⁺ T, and natural killer (NK) cell-dependent cytotoxicity. Our result suggested that cell-based vaccine secreting IL-15:IL-15Rα, may offer the new tools for immunotherapy to treat cancer.

• Korean Journal of Veterinary Research
• /
• v.43 no.2
• /
• pp.211-218
• /
• 2003

Human ovarian cancerous cells survive in a way that they trigger the nucleotide excision repair (NER) or double-strand DNA repair (dsDNA) repair mechanism to show resistance to anticancer drugs and activate many kinds of repair protein, thus removing damaged DNAs. Two experiments on the PA-1 human ovarian teratocareinoma cell line that hardly has any expression of epidermal growth factor receptor (EGFR) were conducted in the study; first, EGF-R was transfected and its receptor was obtained. The receptor was investigated in terms of its mutual relations with many kinds of protein concerning NER or dsDNA repair. Second, it was examined what kind impact cisplatin and adriamycin had on the effects of EGF-R over the PA-1 cell line lacking EGF-R. When being administered with cisplatin and adriamycin, Hey and Hey C2 cell lines showed a high level of resistance while PA-1 cell line a high level of sensitivity. Hey and Hey C2 cell lines that are resistant against anticancer drugs exhibited a high level of EGF-R expression while PA-1 cell line that is sensitive to them did a much lower level of the expression. When PA-1 cell line was transfected for the expression of DNA adduct and EGF-R, it showed a higher level of resistance compared to the control group. There was no difference in the expression of DNA repair proteins (DNA- dependent protein kinase, Ku70, and Ku80) between Hey and the PA-1 cell lines. The results indicate that the Hey cell line that is resistant against cisplatin and adriamycin works along the signaling system responding to the changes of EGF-R while the PA-1 cell line that is sensitive to both of them does to the lack of EGF-R.