• Asian-Australasian Journal of Animal Sciences
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• v.13 no.1
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• pp.115-125
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• 2000

In recent years a great deal of information has accumulated for livestock on vitamin. function, metabolism and supplemental needs. The role of the antioxidant "vitamins" (carotenoids, vitamin E and vitamin C) in immunity and health of livestock has been a fruitful area of research. These nutrients play important roles in animal health by inactivating harmful free radicals produced through normal cellular activity and from various stressors. Both in vitro and in vivo studies showed that these antioxidant vitamins generally enhance different aspects of cellular and noncellular immunity. A compromised immune system will result in reduced animal production efficiency through increased susceptibility to diseases, thereby leading to increased animal morbidity and mortality. Vitamin E has been shown to increase performance of feedlot cattle and to increase immune response for ruminant health, including being beneficial for mastitis control. Vitamin E given to finishing cattle at higher than National Research Council (NRC) requirements dramatically maintained the red color (oxymyoglobin) compared with the oxidized metmyoglobin of beef. Under commercial livestock and poultry production conditions, vitamin allowances higher than NRC requirements may be needed to allow optimum performance. Generally, the optimum vitamin supplementation level is the quantity that achieves the best growth rate, feed utilization, health (including immune competency), and provides adequate body reserves.

• Asian-Australasian Journal of Animal Sciences
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• v.19 no.9
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• pp.1335-1341
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• 2006

We selected a Lactobacillus spp. from Korean healthy infant feces based upon their antioxidant activity. This strain was identified as Lactobacillus gasseri by 16S rDNA sequencing, and named Lactobacillus gasseri NLRI-312. In the present study, we investigate the protective effect of this strain on the $H_2O_2$ induced damage to cellular membrane lipid and DNA in Jurkat cells. To estimate the extent of cellular lipid peroxidation inhibition, MDA (malondialdehyde) was measured, and DNA damage was tested by the comet assay. We also examined probiotic properties including tolerance to acid and bile, antibiotic resistance. From the results obtained, the supplementation of Jurkat cells with NLRI-312 decreased in DNA damage, while no effect was shown on MDA decrease. In probiotic properties, this strain was resistance to both acid and bile, showed considerably higher survival when incubated in pH 2 or 1% bile salts (w/v). We concluded that the NLRI-312 could be used as potential probiotic bacteria, with the effect of reducing DNA damage induced by $H_2O_2$.

• BMB Reports
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• v.43 no.5
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• pp.305-310
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• 2010

Syndecans, cell surface heparansulfate proteoglycans, have been proposed to act as cell surface receptors and/or coreceptors to play critical roles in multiple cellular functions. However, recent reports suggest that the function of syndecans can be further extended through shedding, a cleavage of extracellular domain. Shedding constitutes an additional level for controlling the function of syndecans, providing a means to attenuate and/or regulate amplitude and duration of syndecan signals by modulating the activity of syndecans as cell surface receptors. Whether these remaining cleavage products are still capable of functioning as cell surface receptors to efficiently transduce signals inside of cells is not clear. However, shedding transforms cell surface receptor syndecans into soluble forms, which, like growth factors, may act as novel ligands to induce cellular responses by association with other cell surface receptors. It is becoming interestingly evident that shed syndecans also contribute significantly to syndecan functions in cancer biology. This review presents current knowledge about syndecan shedding and its functional significance, particularly in the context of cancer.

• The Korean Journal of Physiology and Pharmacology
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• v.1 no.4
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• pp.457-466
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• 1997

The effects of DFMO or/and putrescine on the dexamethasone-induced apoptosis of CEM cells were studied to investigate the role of polyamines in anti-leukemic glucocorticoid action. Dexamethasone- induced apoptosis was preceded by significant decreases of cellular polyamine contents and putrescine uptake activity. But DFMO produced decreases of putrescine and spermidine contents and marked increase of putrescine uptake activity, but did not induce apoptosis. However, dexamethasone and DFMO, respectively, induced $G_1-arrest$ in cell cycle and hypophosphorylation of pRb, resulting in the increase of $G_1$ to S ratio and decrease of CEM cell count. DFMO enhanced the dexamethasone-induced apoptosis and $G_1-arrest$. On the other hand, putrescine little affected the apoptotic and $G_1-arresting$ activities of dexamethasone, but almost suppress the effects of DFMO and also the DFMO-dependent enhancement of dexamethasone effects. These results suggested that the dexamethasone-induced apoptosis to be associated with pRb hypophosphorylation and $G_1-arrest$ in CEM cells might be ascribed to the concomitant decreases of cellular polyamine contents and putrescine uptake activity.

• Molecules and Cells
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• v.22 no.2
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• pp.203-209
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• 2006

TBP (TATA-binding protein)-related factor 2 (TRF2) regulates transcription during a nuber of cellular processes. We previously demonstrated that it is localized in the cytoplasm and is translocated to the nucleus by DNA-damaging agents. However, the cytoplasmic localization of TRF2 is controversial. In this study, we reconfirmed its cytoplasmic localization in various ways and examined its nuclear migration. Stresses such as heat shock, redox agents, heavy metals, and osmotic shock did not affect localization whereas genotoxins such as methyl methanesulfonate (MMS), cisplatin, etoposide, and hydroxyurea caused it to migrate to the nucleus. Adriamycin, mitomycin C and ${\gamma}$-rays had no obvious effect. We determined optimal conditions for the nuclear migration. The proportions of cells with nuclei enriched for TRF2 were 25-60% and 5-10% for stressed cells and control cells, respectively. Nuclear translocation was observed after 1 h, 4 h and 12 h for cisplatin, etoposide and MMS and hydroxyurea, respectively. The association of TRF2 with the chromatin and promoter region of the proliferating cell nuclear antigen (PCNA) gene, a putative target of TRF2, was increased by MMS treatment. Thus TRF2 may be involved in genotoxin-induced transcriptional regulation.

• Molecules and Cells
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• v.19 no.1
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• pp.23-30
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• 2005

Spinocerebellar ataxia type 1 (SCA1) is an autosomal-dominant neurodegenerative disorder caused by expansion of the polyglutamine tract in the SCA1 gene product, ataxin-1. Using d2EGFP, a short-lived enhanced green fluorescent protein, we investigated whether polyglutamine-expanded ataxin-1 affects the function of the proteasome, a cellular multicatalytic protease that degrades most misfolded proteins and regulatory proteins. In Western blot analysis and immunofluorescence experiments, d2EGFP was less degraded in HEK 293T cells transfected with ataxin-1(82Q) than in cells transfected with lacZ or empty vector controls. To test whether the stability of the d2EGFP protein was due to aggregation of ataxin-1, we constructed a plasmid carrying $ataxin-1-{\Delta}114$, lacking the self-association region (SAR), and examined degradation of the d2EGFP. Both the level of $ataxin-1-{\Delta}114$ aggregates and the amount of d2EGFP were drastically reduced in cells containing $ataxin-1-{\Delta}114$. Furthermore, d2EGFP localization experiments showed that polyglutamine-expanded ataxin-1 inhibited the general function of the proteasome activity. Taken together, these results demonstrate that polyglutamine-expanded ataxin-1 decreases the activity of the proteasome, implying that a disturbance in the ubiquitin-proteasome pathway is directly involved in the development of spinocerebellar ataxia type1.

• Maxillofacial Plastic and Reconstructive Surgery
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• v.27 no.2
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• pp.110-122
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• 2005

Adenoid cystic carcinoma (ACC) of salivary glands has a protracted clinical course with perineural invasion, delayed onset of hematogenous metastasis, and poor responses to classical cytotoxic chemotherapic agents. Most deaths from salivary ACC are caused by lung metastases that are resistant to conventional therapy. Therefore, knowledge of cellular properties and tumor-host interactions that influence the dissemination of metastatic cells is important for the design of more effective therapy of salivary cancer. I determined in vitro expression of epidermal growth factor receptor (EGFR) and its downstream effectors and vascular endothelial growth factor receptor (VEGFR)-2 on a human salivary ACC cell line (ACC2). I also evaluated the expression of EGF and VEGF signaling molecules and metastasis-related proteins on human salivary ACC cells orthotopically growing in nude mice. In Western blot and immunohistochemical analyses, EGFR and VEGFR-2 were presented and phosphorylated in ACC2 cells. In human parotid cancer xenografts in nude mice, EGF and VEGF signaling molecules, IL-8, and MMP-9 were expressed at markedly higher levels than in normal parotid tissues. Moreover, tumor-associated endothelial cells of this orthotopic parotid tumor expressed phosphorylated VEGFR-2 and phosphorylated Akt, which is a cell-survival protein. These data show that those biomarkers can be molecular targets for therapy of salivary ACC, which has a propensity for delayed lung metastasis.

• CELLMED
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• v.12 no.3
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• pp.14.1-14.2
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• 2022

Currently, a 70-year-old woman started suffering from S.I joint pain from 1973 and had severe pain in the S.I joint, wrist, and elbow from 1975 to 1977, and was diagnosed with spinal tuberculosis at a general hospital. From 1978 to 1987, she suffered from chronic fatigue and insomnia, and since January 1, 1988, she was unable to get up while lying down, suffering from whole body joint, muscle pain, and fibromyalgia. In May 1989, she was also diagnosed with ankylosing spondylitis through genetic testing at the Catholic St. Mary's Hospital Rheumatology Department in Korea, and was treated with sulfasalazine, analgesic, and immunosuppressant, methotrexate, for 12 years until 1999, but none of the drugs eliminated the pain. She was hospitalized and discharged repeatedly, and continued to receive salt water poultice and exercise therapy at home, but was unable to move at all. In 2000, after biologic treatment with Remicade injection (Remsima®), she was able to walk and move, and after that, she was continuously prescribed biologics. From 2015 to 2019, Enbrel® (Etanercept) injection was prescribed once a week, but the symptoms such as severe pain (joint and muscle, fibromyalgia), scleroderma, Sjogren's syndrome (dryness of eyes, nose and mouth), difficulty swallowing, chronic fatigue, and stiff body appeared. Around January 2018, hepatic indicators were high and lymphocytes became enlarged. However, most serious injuries were highly improved after the OCNT combination therapy using active phytonutrients, anthocyanin-fucoidan nanocomplex. Therefore, for patients with such experiences, OCNT treatment is proposed as an alternative.

• Journal of the Korean Crystal Growth and Crystal Technology
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• v.11 no.4
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• pp.170-175
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• 2001

It was possible to grow the $Al_{2}O_{3}$ based $Y_{3}A_{5}O_{12}(YAG),ZrO_{2}$ binary and ternary eutectic fibers using micro-pulling down method with a growing rate of 0.1~15 mm/min. While $Al_{2}O_{3}/ZrO_{2}$ showed cellular-lamellar structure, $Al_{2}O_{3}$/YAG and $Al_{2}O_{3}$/YAG/$ZrO_{2}$ternary eutectic fibers showed homogeneous Chinese script lamellar structures. The microstructures of $Al_{2}O_{3}/ZrO_{2}$ binary eutectic fibers changed with solidification rate from lamellar pattern to cellular structure. The interlamellar spacing agreed with the inverse-square-root dependance on pulling rate according to $\lambda$=$kv_p\;{-1/2}$. $Al_{2}O_{3}/ZrO_{2}$ binary eutectic fibers recorded the highest tensile strength of about 1560MPa at room temperature. $Al_2O_3/YAG/ZrO_2$ternary eutectic fiber showed excellent thermal stability to $1200^{\circ}C$ without significant decrease. The maximum strength of ternary eutectic fibers recorded were 1100MPa at $25^{\circ}C$ and 970MPa at $1200^{\circ}C$, respectively.

• IMMUNE NETWORK
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• v.21 no.1
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• pp.3.1-3.16
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• 2021

Coronavirus disease 2019 caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has been spreading worldwide since its outbreak in December 2019, and World Health Organization declared it as a pandemic on March 11, 2020. SARS-CoV-2 is highly contagious and is transmitted through airway epithelial cells as the first gateway. SARS-CoV-2 is detected by nasopharyngeal or oropharyngeal swab samples, and the viral load is significantly high in the upper respiratory tract. The host cellular receptors in airway epithelial cells, including angiotensin-converting enzyme 2 and transmembrane serine protease 2, have been identified by single-cell RNA sequencing or immunostaining. The expression levels of these molecules vary by type, function, and location of airway epithelial cells, such as ciliated cells, secretory cells, olfactory epithelial cells, and alveolar epithelial cells, as well as differ from host to host depending on age, sex, or comorbid diseases. Infected airway epithelial cells by SARS-CoV-2 in ex vivo experiments produce chemokines and cytokines to recruit inflammatory cells to target organs. Same as other viral infections, IFN signaling is a critical pathway for host defense. Various studies are underway to confirm the pathophysiological mechanisms of SARS-CoV-2 infection. Herein, we review cellular entry, host-viral interactions, immune responses to SARS-CoV-2 in airway epithelial cells. We also discuss therapeutic options related to epithelial immune reactions to SARS-CoV-2.