A yeast strain, designated as JAF-11 T , was isolated from flower ofPrunus mume Sieb. et Zucc. in Gwangyang, Republic of Korea. Phylogenetic analysis showed that strain JAF-11 T was closely related to Neodothiora populina CPC 39399 T with 2.07 % sequence divergence (12 nucleotide substitutions and three gaps in 581 nucleotides) in the D1/D2 domain of the large subunit (LSU) rRNA gene, and Rhizosphaera macrospora CBS 208.79 T with 4.66 % sequence divergence (25 nucleotide substitutions and five gaps in 535 nucleotides) in the internal transcribed spacer (ITS) region. Further analysis based on the concatenated sequen ces of the D1/D2 domain of the LSU rRNA gene and the ITS region confirmed that strain JAF-11 T was well-separated from Neodothiora populina CPC 39399 T . In addition to the phylo genetic differences, strain JAF-11 T was distinguished from its closest species, Neodothiora populina CPC 39399 T and Rhizosphaera macrospora CBS 208.79 T belonging to the family Dothioraceae by its phenotypic characteristics, such as assimilation of carbon sources. Hence, the name Neodothiora pruni sp. nov. is proposed with type strain JAF-11 T (KACC 48808 T ; MB 850034).

IL-22, a pleiotropic cytokine, is known to have a profound effect on the regeneration of damaged intestinal barriers. The tissue-protective properties of IL-22 are expected to be potentially exploited in the attenuation and treatment of colitis. However, because of the disease-promoting role of IL-22 in chronic inflammation, a comprehensive evaluation is required to translate IL-22 into the clinical domain. Here, we present the effective production of soluble human IL-22 in bacteria to prove whether recombinant IL-22 has the ability to ameliorate colitis and inflammation. IL-22 was expressed in the form of a biologically active monomer and non-functional oligomers. Monomeric IL-22 (mIL-22) was highly purified through a series of 3 separate chromatographic methods and an enzymatic reaction. We reveal that the resulting mIL-22 is correctly folded and is able to phosphorylate STAT3 in HT-29 cells. Subsequently, we demonstrate that mIL-22 enables the attenuation of dextran sodium sulfate-induced acute colitis in mice, as well as the suppression of pro-inflammatory cytokine production. Collectively, our results suggest that the recombinant mIL-22 is suitable to study the biological roles of endogenous IL-22 in immune responses and can be developed as a biological agent associated with inflammatory disorders.

Purpose: The aim of this study was to compare changes of bite force, occlusal contact area, and dynamic functional occlusion analysis after occlusal stabilization splint therapy during sleep for one month in a patient with bruxism. Materials and Methods: From October 2021 to July 2022, sleep bruxism of 30 patients who visited the Department of Oral Medicine at Yonsei University College of Dentistry Hospital were recruited. The participants were divided into two groups: using an occlusal stabilization splint during sleep (treatment; n = 15) and not using an occlusal stabilization splint (control; n = 15). Before using the occlusal stabilization splint and one month after, bite force, occlusal contact area and dynamic functional occlusion analysis (ratio of left/right bite forces, average bite forces, maximum bite forces, and maximum contact areas during lateral and anterior and posterior mandibular movements) were performed. Results: There was no difference in bite force and occlusal contact area between the treatment group using the occlusal stabilization splint and the control group not using the occlusal stabilization splint during sleep for one month. However, there were significant differences in the average bite force and maximum bite force in the lateral and anterior and posterior mandibular movements and the maximum contact areas in the anterior and posterior mandibular movements. Conclusion The occlusal stabilization splint is helpful for sleep bruxism patients who lateral and anterior and posterior mandibular movements. In addition, further studies are needed a double-blind study with a large population.

Body donation trends in Korea have changed significantly over the last 3 decades. Establishing a body donation system will promote donations to universities for academic purposes. Yonsei University College of Medicine started its own body donation system in 1992, including documenting donors’ records. However, there has been no reported attempt to analyze the trend of these records, which could provide noteworthy information that can be interpreted for medical advances. This study performed a statistical analysis of the donors’ records between 1992 and 2019 to analyze the sociological and anthropological changes. Donor personal information such as sex, age, religion, and place and cause of death were extracted from the Yonsei University College of Medicine database. Our statistical analysis revealed significant correlations between donors’ records and the changes in the number of geriatric hospitals, religious beliefs, number of donations, and donor age.

Body donation trends in Korea have changed significantly over the last 3 decades. Establishing a body donation system will promote donations to universities for academic purposes. Yonsei University College of Medicine started its own body donation system in 1992, including documenting donors’ records. However, there has been no reported attempt to analyze the trend of these records, which could provide noteworthy information that can be interpreted for medical advances. This study performed a statistical analysis of the donors’ records between 1992 and 2019 to analyze the sociological and anthropological changes. Donor personal information such as sex, age, religion, and place and cause of death were extracted from the Yonsei University College of Medicine database. Our statistical analysis revealed significant correlations between donors’ records and the changes in the number of geriatric hospitals, religious beliefs, number of donations, and donor age.

BACKGROUND AND OBJECTIVES: Since Korea has been divided into two countries over 60 years ago and differences has gradually developed between the two, an influx of North Korean refugees to South Korea have soared over the past 20 years. Their complaints regarding taste intensity, particularly about strong sweetness of foods, are common after entry into South Korea. Because a long-term over-exposure or restriction to some taste stimuli causes profound alterations in corresponding taste sensitivity in humans, we hypothesized that sugar restriction, which remains common in North Korea, has influenced sweet sensitivity of North Koreans.SUBJECTS AND METHOD: To test this hypothesis, we assessed the taste stimuli recognition and detection thresholds of both young adults North refugees and South Koreans using a 1-mL whole-mouth gustatory test applied to a series of sweet, bitter, sour, and salty solutions. RESULTS: As expected, the cumulative curve of the recognition threshold for sucrose shifted to the left and the mean recognition threshold for sucrose was significantly lower (0.5357% vs. 0.7393%, p=0.044) for North refugees than for South participants. On the other hand, the recognition threshold for salt was significantly higher (0.2174% vs. 0.1212%, p=0.027) in North refugees. No differences on the recognition taste sensitivity for quinine hydrochloride and citric acid were observed. CONCLUSION The findings documented in the present study indicate that a prolonged food deficit seems to have changed the taste sensitivity of healthy North Korean refugees. The altered taste sensitivity was most pronounced for sweet and salty tastes, and lasted up to 3.5 years after the refugees left North Korea.

PURPOSE: Lapatinib is a candidate drug for treatment of trastuzumab-resistant, human epidermal growth factor receptor 2 (HER2)–positive gastric cancer (GC). Unfortunately, lapatinib resistance renders this drug ineffective. The present study investigated the implication of forkhead box O1 (FOXO1) signaling in the acquired lapatinib resistance in HER2-positive GC cells. MATERIALS AND METHODS: Lapatinib-resistant GC cell lines (SNU-216 LR2-8) were generated in vitro by chronic exposure of lapatinib-sensitive, HER2-positive SNU-216 cells to lapatinib. SNU-216 LR cells with FOXO1 overexpression were generated by stable transfection of a constitutively active FOXO1 mutant (FOXO1A3). HER2 and MET in SNU-216 LR cells were downregulated using RNA interference. The sensitivity of GC cells to lapatinib and/or cisplatin was determined by crystal violet assay. In addition, Western blot analysis, luciferase reporter assay and reverse transcription–polymerase chain reaction were performed. RESULTS: SNU-216 LR cells showed upregulations of HER2 and MET, but downregulation of FOXO1 compared to parental SNU-216 cells. FOXO1 overexpression in SNU-216 LR cells significantly suppressed resistance to lapatinib and/or cisplatin. In addition, FOXO1 negatively controlled HER2 and MET at the transcriptional level and was negatively controlled by these molecules at the post-transcriptional level. A positive crosstalk was shown between HER2 and MET, each of which increased resistance to lapatinib and/or cisplatin. CONCLUSION: FOXO1 serves as an important linker between HER2 and MET signaling pathways through negative crosstalks and is a key regulator of the acquired lapatinib resistance in HER2-positive GC cells. These findings provide a rationale for establishing a novel treatment strategy to overcome lapatinib resistance in a subtype of GC patients.
Blotting, Western ; Cell Line ; Cisplatin ; Down-Regulation ; Drug Resistance ; Gentian Violet ; Humans ; In Vitro Techniques ; Luciferases ; Parents ; Receptor, Epidermal Growth Factor ; Receptor, ErbB-2 ; RNA Interference ; Stomach Neoplasms ; Transfection ; Up-Regulation

BACKGROUND/OBJECTIVES: The objective of this study was to investigate the effects of vitamin C on inflammation, tumor development, and dysbiosis of intestinal microbiota in an azoxymethane (AOM)/dextran sulfate sodium (DSS)-induced inflammation-associated early colon cancer mouse model. MATERIALS/METHODS: Male BALB/c mice were injected intraperitoneally with AOM [10 mg/kg body weight (b.w)] and given two 7-d cycles of 2% DSS drinking water with a 14 d inter-cycle interval. Vitamin C (60 mg/kg b.w. and 120 mg/kg b.w.) was supplemented by gavage for 5 weeks starting 2 d after the AOM injection. RESULTS: The vitamin C treatment suppressed inflammatory morbidity, as reflected by disease activity index (DAI) in recovery phase and inhibited shortening of the colon, and reduced histological damage. In addition, vitamin C supplementation suppressed mRNA levels of pro-inflammatory mediators and cytokines, including cyclooxygenase-2, microsomal prostaglandin E synthase-2, tumor necrosis factor-α, Interleukin (IL)-1β, and IL-6, and reduced expression of the proliferation marker, proliferating cell nuclear antigen, compared to observations of AOM/DSS animals. Although the microbial composition did not differ significantly between the groups, administration of vitamin C improved the level of inflammation-related Lactococcus and JQ084893 to control levels. CONCLUSION: Vitamin C treatment provided moderate suppression of inflammation, proliferation, and certain inflammation-related dysbiosis in a murine model of colitis associated-early colon cancer. These findings support that vitamin C supplementation can benefit colonic health. Long-term clinical studies with various doses of vitamin C are warranted.
Animals ; Ascorbic Acid* ; Azoxymethane* ; Body Weight ; Colitis ; Colon* ; Colonic Neoplasms* ; Cyclooxygenase 2 ; Cytokines ; Drinking Water ; Dysbiosis ; Gastrointestinal Microbiome ; Humans ; Inflammation ; Interleukin-6 ; Interleukins ; Lactococcus ; Male ; Mice* ; Microbiota ; Necrosis ; Proliferating Cell Nuclear Antigen ; RNA, Messenger ; Sodium* ; Vitamins*

PURPOSE: We previously reported that forkhead transcription factors of the O class 1 (FOXO1) expression in gastric cancer (GC) was associated with angiogenesis-related molecules. However, there is little experimental evidence for the direct role of FOXO1 in GC. In the present study, we investigated the effect of FOXO1 on the tumorigenesis and angiogenesis in GC and its relationship with SIRT1. MATERIALS AND METHODS: Stable GC cell lines (SNU-638 and SNU-601) infected with a lentivirus containing FOXO1 shRNA were established for animal studies as well as cell culture experiments. We used xenograft tumors in nude mice to evaluate the effect of FOXO1 silencing on tumor growth and angiogenesis. In addition, we examined the association between FOXO1 and SIRT1 by immunohistochemical tissue array analysis of 471 human GC specimens and Western blot analysis of xenografted tumor tissues. RESULTS: In cell culture, FOXO1 silencing enhanced hypoxia inducible factor-1alpha (HIF-1alpha) expression and GC cell growth under hypoxic conditions, but not under normoxic conditions. The xenograft study showed that FOXO1 downregulation enhanced tumor growth, microvessel areas, HIF-1alpha activation and vascular endothelial growth factor (VEGF) expression. In addition, inactivated FOXO1 expression was associated with SIRT1 expression in human GC tissues and xenograft tumor tissues. CONCLUSION: Our results indicate that FOXO1 inhibits GC growth and angiogenesis under hypoxic conditions via inactivation of the HIF-1alpha-VEGF pathway, possibly in association with SIRT1. Thus, development of treatment modalities aiming at this pathway might be useful for treating GC.
Angiogenesis Modulating Agents ; Animals ; Anoxia ; Blotting, Western ; Carcinogenesis ; Cell Culture Techniques ; Cell Line ; Down-Regulation ; Forkhead Transcription Factors ; Heterografts ; Humans ; Lentivirus ; Mice ; Mice, Nude ; Microvessels ; RNA, Small Interfering ; Stomach Neoplasms* ; Tissue Array Analysis ; Transcription Factors* ; Vascular Endothelial Growth Factor A

BACKGROUND: Oxidative stress plays an important role in the pathogenesis of inflammatory bowel disease. The objective of this study is to investigate the protective effect of Sasa quelpaertensis leaf extract (SQE) against oxidative stress in mice with dextran sulfate sodium (DSS)-induced colitis. METHODS: Mice were treated with SQE (100 mg/kg or 300 mg/kg body weight) by gavage in advance two weeks before inflammation was induced. Then, the mice were administered with 2.5% DSS in drinking water for 7 days and normal drinking water for 7 days between two DSS treatment. Disease activity index values, gut motility, and severity of the resulting oxidative DNA damage were analyzed. The antioxidant effect of SQE was evaluated by measuring malondialdehyde (MDA) and superoxide dismutase (SOD) activity in plasma samples. Catalase activity and expressions levels of glutathione peroxidase 1 (Gpx1), SOD1, and SOD2 were also detected in colon tissues. RESULTS: Administration of SQE significantly reduced the severity of DSS-induced colitis compared to the control (Ctrl) group. Levels of 8-oxo-dG, an oxidative DNA damage marker, were significantly lower in the SQE group compared to the untreated DSS Ctrl group. In the SQE (300 mg/kg) group, MDA levels were significantly lower, while SOD and catalase activity levels in the plasma samples were significantly higher compared with the DSS Ctrl group. The expression levels of the antioxidant enzymes, SOD2 and Gpx1, were significantly higher, while the levels of SOD 1 expression were lower, in the colon tissues of the DSS Ctrl group compared with those of the Ctrl group. In contrast, administration of SQE significantly down-regulated SOD2 and Gpx1 expressions and up-regulated SOD1 expression. CONCLUSIONS: These results indicate that SQE efficiently suppresses oxidative stress in DSS-induced colitis in mice, and its action is associated with the regulation of antioxidant enzymes.
Animals ; Antioxidants ; Catalase ; Colitis* ; Colon ; Dextran Sulfate* ; Dextrans* ; DNA Damage ; Drinking Water ; Glutathione Peroxidase ; Inflammation ; Inflammatory Bowel Diseases ; Malondialdehyde ; Mice* ; Oxidative Stress ; Plasma ; Sasa* ; Superoxide Dismutase