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Kim, Hyemin,Bae, Seyeon,Kim, Yejin,Cho, Chung-Hyun,Kim, Sung Joon,Kim, Yong-Jin,Lee, Seung-Pyo,Kim, Hang-Rae,Hwang, Young-il,Kang, Jae Seung,Lee, Wang Jae Elsevier 2013 FREE RADICAL BIOLOGY AND MEDICINE Vol.65 No.-
<P><B>Abstract</B></P> <P>It is thought that vitamin C has protective roles on stress-induced heart damage and the development of cardiovascular diseases, but its precise role and mechanisms are unclear. In the present study, we investigated the specific mechanisms by which vitamin C leads to protecting the heart from stress-induced damage in the <I>Gulo(</I>−/−<I>)</I> mice which cannot synthesize vitamin C like humans. By exposure to stress (1h/day), the heartbeat and cardiac output in vitamin C-insufficient <I>Gulo(</I>−/−<I>)</I> mice were definitely decreased, despite a significant increase of adrenaline (ADR) and noradrenaline (NA) production. A change of cardiac structure caused by the death of cardiomyocytes and an increased expression of matrix metalloprotease (MMP)-2 and -9 were also found. Moreover, lipid peroxidation and the production of tumor necrosis factor-alpha (TNF-α) in the heart were increased. Finally, all vitamin C-insufficient <I>Gulo(</I>−/−<I>)</I> mice were expired within 2 weeks. Interestingly, all of the findings in vitamin C-insufficient <I>Gulo(</I>−/−<I>)</I> mice were completely prevented by the supplementation of a sufficient amount of vitamin C. Taken together, vitamin C insufficiency increases the risk of stress-induced cardiac damage with structural and functional changes arising from the apoptosis of cardiomyocytes.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Vitamin C insufficiency accelerates the stress-induced death of <I>Gulo(</I>−/−<I>)</I> mice. </LI> <LI> Oxidative stress in the heart is increased by stress and vitamin C insufficiency. </LI> <LI> TNF-α, ADR, and NA are excessively produced by stress and vitamin C insufficiency. </LI> <LI> Structural/functional cardiac changes are induced by stress and vitamin C insufficiency. </LI> <LI> Vitamin C supplementation prevents cardiac changes and death of <I>Gulo(</I>−/−<I>)</I> mice. </LI> </UL> </P>
Hyemin Kim,Soyoung Lee,Ji-Won Kim,Ju-Yang Jung,Chang-Hee Suh,Hyoun-Ah Kim 대한내과학회 2024 The Korean Journal of Internal Medicine Vol.39 No.1
Background/Aims: This study aimed to identify the clinical characteristics of patients with concurrent rheumatoid arthritis (RA) and suspected non-tuberculous mycobacterial (NTM) infections as well as determine their prognostic factors. Methods: We retrospectively reviewed the medical records of 91 patients with RA whose computed tomography (CT) findings suggested NTM infection. Subsequently, we compared the clinical characteristics between patients with and without clinical or radiological exacerbation of NTM-pulmonary disease (PD) and investigated the risk factors for the exacerbation and associated mortality. Results: The mean age of patients with RA and suspected NTM-PD was 65.0 ± 10.2 years. The nodular/bronchiectatic (NB) form of NTM-PD was the predominant radiographic feature (78.0%). During follow-up, 36 patients (41.9%) experienced a radiological or clinical exacerbation of NTM-PD, whereas 12 patients (13.2%) died. Combined interstitial lung disease (ILD), microbiologically confirmed NTM-PD, and NB with the fibrocavitary (FC) form on chest CT were identified as risk factors for the clinical or radiological exacerbation of NTM-PD. Hydroxychloroquine use was identified as a good prognostic factor. Conversely, history of tuberculosis, ILD, smoking, microbiologically confirmed NTM-PD, and NB with the FC form on chest CT were identified as poor prognostic factors for mortality in suspected NTM-PD. Conclusions: ILD and NB with the FC form on chest CT were associated with NTM-PD exacerbation and mortality. Hydroxychloroquine use may lower the risk of NTM-PD exacerbation. Therefore, radiographic features and presence of ILD should be considered when predicting the prognosis of patients with RA and suspected NTM-PD.
Antioxidant and Probiotic Properties of Lactobacilli and Bifidobacteria of Human Origins
Hyemin Kim,Jin-Seong Kim,YongGyeong Kim,Yulah Jeong,Ji-Eun Kim,백남수,강창호 한국생물공학회 2020 Biotechnology and Bioprocess Engineering Vol.25 No.3
Oxidative stress can cause various diseases including inflammation, neurological disorders, cancer, diabetes, and cardiovascular diseases. Due to the current search for natural antioxidants, probiotics have received increasing scientific interest and are facing a growing industrial demand. Although various strains of lactobacilli and bifidobacteria are currently used in numerous health food supplements, their antioxidative activities have been relatively poorly identified. Therefore, in this work, we evaluated the in vitro effect of antioxidative activities (through assays of 2,2-diphenyl-1-picrylhydrazyl (DPPH) and 2,2′-azinobis-(3-ethylbenzothiazoline-6-sulfonate) (ABTS) radical scavenging) and probiotic functional properties (cell viability in a simulated gastrointestinal tract, enzyme production, carbohydrate availability, and safety assessments) of Lactobacillus spp. and Bifidobacterium spp. isolated from human origins. From the nitric oxide (NO) assay screening, four strains (Bifidobacterium animalis subsp. lactis MG741, B. breve MG729, L. reuteri MG505, and L. rhamnosus MG316) were selected based on the yield amount of ferment productivity (> × 1010 CFU/g) and showed high antioxidant activities ranging from 22.2% to 38.2% in DPPH free radical scavenging, and 50.0% to 93.6% in ABTS radical scavenging. Regarding their functional properties as probiotics, these four strains were resistant to simulated gastric (pH 3 and 4) and intestinal fluids (pH 7 and 8), and showed potential for the promotion of health based on hemolysis, auto-aggregation, antibiotic susceptibility, enzyme production, and biochemical profiles. Altogether, our results showed that the selected probiotic strains may be good candidates as food ingredients to mitigate oxidative stress-related symptoms.
Kim, Hyemin,Kim, Ji-Woo,Kim, So-Jin,Choi, Young-Jun,Kim, Dae-Sung,Park, Han-Jin Elsevier 2018 Stem cell research Vol.26 No.-
<P>Pregnane X receptor (PXR) is a key nuclear receptor that mediates drug metabolism and stimulates hepatocyte proliferation. However, the lack of PXR expression in human pluripotent stem cell-derived hepatocytes limits their application for drug screening and toxicity testing. Here, we generated a PXR-mCherry reporter human induced pluripotent stem cell (hiPSC) line using the CRISPR/Cas9 system. PXR-mCherry hiPSCs were pluripotent and had differentiation potential and a normal karyotype. This cell line is an important tool for identifying factors that increase PXR-mediated drug metabolism and hepatocyte proliferation. (C) 2017 The Authors. Published by Elsevier B.V.</P>
Kim, Ha Na,Kim, Hyemin,Kong, Joo Myung,Bae, Seyeon,Kim, Yong Sung,Lee, Naeun,Cho, Byung Joo,Lee, Seung Koo,Kim, Hang‐,Rae,Hwang, Young‐,il,Kang, Jae Seung,Lee, Wang Jae Wiley Subscription Services, Inc., A Wiley Company 2011 Journal of cellular biochemistry Vol.112 No.3
<P><B>Abstract</B></P><P>It is known that vitamin C induces apoptosis in several kinds of tumor cells, but its effect on the regulation of the angiogenic process of tumors is not completely studied. Vascular endothelial growth factor (VEGF) is the most well‐known angiogenic factor, and it has a potent function as a stimulator of endothelial survival, migration, as well as vascular permeability. Therefore, we have investigated whether vitamin C can regulate the angiogenic process through the modulation of VEGF production from B16F10 melanoma cells. VEGF mRNA expression and VEGF production at protein levels were suppressed by vitamin C. In addition, we found that vitamin C suppressed the expression of cyclooxygenase (COX)‐2 and that decreased VEGF production by vitamin C was also restored by the administration of prostaglandin E2 which is a product of COX‐2. These results suggest that vitamin C suppresses VEGF expression via the regulation of COX‐2 expression. Mitogen‐activated protein kinases are generally known as key mediators in the signaling pathway for VEGF production. In the presence of vitamin C, the activation of p42/44 MAPK was completely inhibited. Taken together, our data suggest that vitamin C can down‐regulate VEGF production via the modulation of COX‐2 expression and that p42/44 MAPK acts as an important signaling mediator in this process. J. Cell. Biochem. 112: 894–901, 2011. © 2010 Wiley‐Liss, Inc.</P>
Burkitt Lymphoma Initially Presenting as Acute Pancreatitis in an Adolescent Boy
Hyemin Kim,Yiyoung Kwon,Eun Sil Kim,Hee Young Ju,구홍회,최연호,Mi Jin Kim 대한소아혈액종양학회 2020 Clinical Pediatric Hematology-Oncology Vol.27 No.2
In children and adolescents, acute pancreatitis is a rare cause of abdominal pain. The causes of pancreatitis in children are various including infection and drugs, but the overall cause of this condition in a pediatric patient is sometimes unknown. We describe a case of Burkitt lymphoma which showed acute pancreatitis findings as an initial presentation. In this case, a 16-year-old boy presented with abdominal pain in the left upper quadrant that had been present for one month. Pancreatitis was suspected due to high amylase and lipase and the computed tomography findings in the patient, which showed swelling and adjacent infiltration of the pancreas. However, initial treatments did not improve the patient’s symptoms. The following imaging studies showed mass-like lesions involving the pancreas, distal duodenum and jejunum associated with mesenteric lymphadenopathy that suggested a lymphoma in this case. In the final analysis, the patient was diagnosed with Burkitt lymphoma which was seen on bone marrow biopsies and also found on the small bowel tissue biopsies.
Kim, Yeryung,Kim, Hyemin,Yoo, Hae-Young,Kang, Jae Seung,Kim, Sung Joon,Kim, Jin Kyoung,Cho, Hyun Sung The Korean Academy of Medical Sciences 2011 JOURNAL OF KOREAN MEDICAL SCIENCE Vol.26 No.3
<P>Hyperoxic ventilation induces detrimental effects on the respiratory system, and ambient oxygen may be harmful unless compensated by physiological anti-oxidants, such as vitamin C. Here we investigate the changes in electrolyte transport of airway epithelium in mice exposed to normobaric hyperoxia and in gulonolacton oxidase knock-out (gulo[-/-]) mice without vitamin C (Vit-C) supplementation. Short-circuit current (I<SUB>sc</SUB>) of tracheal epithelium was measured using Ussing chamber technique. After confirming amiloride-sensitive Na<SUP>+</SUP> absorption (ΔI<SUB>sc,amil</SUB>), cAMP-dependent Cl<SUP>-</SUP> secretion (ΔI<SUB>sc,forsk</SUB>) was induced by forskolin. To evaluate Ca<SUP>2+</SUP>-dependent Cl<SUP>-</SUP> secretion, ATP was applied to the luminal side (ΔI<SUB>sc,ATP</SUB>). In mice exposed to 98% PO<SUB>2</SUB> for 36 hr, ΔI<SUB>sc,forsk</SUB> decreased, ΔI<SUB>sc,amil</SUB> and ΔI<SUB>sc,ATP</SUB> was not affected. In gulo(-/-) mice, both ΔI<SUB>sc,forsk</SUB> and ΔI<SUB>sc,ATP</SUB> decreased from three weeks after Vit-C deprivation, while both were unchanged with Vit-C supplementation. At the fourth week, tissue resistance and all electrolyte transport activities were decreased. An immunofluorescence study showed that the expression of cystic fibrosis conductance regulator (CFTR) was decreased in gulo(-/-) mice, whereas the expression of KCNQ1 K<SUP>+</SUP> channel was preserved. Taken together, the CFTR-mediated Cl<SUP>-</SUP> secretion of airway epithelium is susceptible to oxidative stress, which suggests that supplementation of the antioxidant might be beneficial for the maintenance of airway surface liquid.</P>