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The senescence-induced staygreen protein regulates chlorophyll degradation.
Park, So-Yon,Yu, Jae-Woong,Park, Jong-Sung,Li, Jinjie,Yoo, Soo-Cheul,Lee, Na-Yeoun,Lee, Sang-Kyu,Jeong, Seok-Won,Seo, Hak Soo,Koh, Hee-Jong,Jeon, Jong-Seong,Park, Youn-Il,Paek, Nam-Chon American Society of Plant Physiologists 2007 The Plant cell Vol.19 No.5
<P>Loss of green color in leaves results from chlorophyll (Chl) degradation in chloroplasts, but little is known about how Chl catabolism is regulated throughout leaf development. Using the staygreen (sgr) mutant in rice (Oryza sativa), which maintains greenness during leaf senescence, we identified Sgr, a senescence-associated gene encoding a novel chloroplast protein. Transgenic rice overexpressing Sgr produces yellowish-brown leaves, and Arabidopsis thaliana pheophorbide a oxygenase-impaired mutants exhibiting a stay-green phenotype during dark-induced senescence have reduced expression of Sgr homologs, indicating that Sgr regulates Chl degradation at the transcriptional level. We show that the leaf stay-greenness of the sgr mutant is associated with a failure in the destabilization of the light-harvesting chlorophyll binding protein (LHCP) complexes of the thylakoid membranes, which is a prerequisite event for the degradation of Chls and LHCPs during senescence. Transient overexpression of Sgr in Nicotiana benthamiana and an in vivo pull-down assay show that Sgr interacts with LHCPII, indicating that the Sgr-LHCPII complexes are formed in the thylakoid membranes. Thus, we propose that in senescing leaves, Sgr regulates Chl degradation by inducing LHCPII disassembly through direct interaction, leading to the degradation of Chls and Chl-free LHCPII by catabolic enzymes and proteases, respectively.</P>
Park, Joon Seok,Kang, In Kyu,Park, Jong Hwa,Park, Joo Kyung,Kim, Hong Taek,Yoon, Soon Jong Trans Tech Publications, Ltd. 2010 Materials science forum Vol.654 No.-
<P>In construction industries, new construction materials are needed to overcome some problems associated with the use of conventional construction materials due to the change of environmental and social requirements. Accordingly, the requirements to be satisfied in the design of civil engineering structures are diversified. As a new construction material in the civil engineering industries, fiber reinforced polymeric plastic (FRP) has a superior corrosion resistance, high specific strength/stiffness, etc. Therefore, such properties can be used to mitigate the problems associated with the use of conventional construction materials. Nowadays, new types of bridge piers and marine piles are being studied for new construction. They are made of concrete filled fiber reinforced polymeric plastic tubes (CFFT). In this paper, a new type of FRP-concrete composite pile which is composed of reinforced concrete filled FRP tube (RCFFT) is proposed to improve compressive strength as well as flexural strength of an RCFFT. The load carrying capacity of proposed RCFFT is discussed based on the result of experimental and analytical investigations.</P>
Park, Chun-Woong,Rhee, Yun-Seok,Go, Byung-Wook,Kam, Sung-Hoon,Lee, Kyu-Hyun,Lee, Hye-Suk,Park, Eun-Seok 대한약학회 2008 Archives of Pharmacal Research Vol.31 No.9
A simple and sensitive HPLC method for the analysis of rabeprazole in plasma is described using UV detection in the presence of lorazepam as the internal standard. Rabeprazole and lorazepam were extracted with ethyl ether and quantitated using a reverse-phase $C_{18}$ column. The method was specific as there were no interfering peaks in the human plasma eluting at the retention times of rabeprazole and lorazepam. The method was fully validated in human plasma for the concentration range of 20.0-1000.0 ng/ml. The correlation coefficients were greater than 0.999. Extraction recoveries were 72.3% for the drug and 79.1% for the internal standard. The method was simple, reliable, and accurate for the quantitation of rabeprazole in human plasma. The same plasma samples, which were collected in healthy male volunteers administered a 20 mg tablet of $Pariet^{(R)}$, were analyzed by HPLC and LC/MS/MS. As a result of that, there was no significant difference between pharmacokinetic parameters. The suitability of HPLC method for pharmacokinetic studies was verified by determining the relevant pharmacokinetic parameters.
Endoscopic disconnection of hypothalamic astrocytoma causing gelastic epilepsy
Park, Young Seok,Lee, Yun Ho,Shim, Kyu-Won,Kim, Dong-Seok,Lee, Joon Soo,Kim, Heung Dong Journal of Neurosurgery Publishing Group 2009 Journal of neurosurgery. Pediatrics Vol.4 No.2
<P>The authors report on a case of juvenile pilocytic astrocytoma (JPA) and concomitant hypothalamic hamartoma (HH) with gelastic epilepsy that was successfully treated with endoscopic disconnection. This 6-year-old girl presented with prolonged, medically intractable gelastic seizures that were often followed by generalized tonic seizures. An enhancing, low-grade hypothalamic tumor was identified on MR images obtained when she was 11 months old, but no surgical intervention was attempted at that time apart from bur hole drainage of a chronic subdural hemorrhage. In the first surgery, performed when she was 6 years of age, the authors attempted disconnection and tumor sampling; the lesion was revealed to be a JPA. A second endoscopic disconnection was performed 1 year later to improve seizure control and obtain a pathological specimen from the nonenhancing contralateral side. The pathological results after the second surgery revealed that the enhancing mass was a spontaneously regressing JPA and the contralateral nonenhancing mass was an HH. The HH was found as latent tumor and the JPA was the mass causing gelastic epilepsy. To the authors' knowledge, this is the first report of a patient with a spontaneously regressing JPA and concomitant HH, both of which were treated by endoscopic disconnection.</P>
Park, Seung-Taeck,Park, Yang-Kyu,Park, Jae-Hwang,Cho, Kwang-Ho,Ryu, Do-Gon,Jeon, Byung-Hoon,Shin, Min-Kyo,Han, Du-Seok,Cho, Nam-Su,Shin, Dong-Min Kyung Hee Oriental Medicine Research Center 2000 International journal of oriental medicine Vol.1 No.1
Effects of Rhizoma gastrodiae on glucose oxidase-induced neurotoxicity was investigated in cultured newborn mouse spinal dorsal root ganglion(DRG) neurons that were treated in the media with or without glucose oxidase. In addition, the protective effect of Rhizoma gastrodiae extract against glucose oxidase-induced neurotoxicity was examined. Cytotoxic values were expressed as a percentage of number of living cells by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. In this paper, exposure of neurons to glucose oxidase resulted in a significant call death in a dose- and time-dependent manners in DRG neuron cultures. The decrease in cell viability induced by the glucose oxidase was blocked by Rhizoma gastrodiae extract. These results indicate that the neuroprotective effect of Rhizoma gastrodiae extract against glucose oxidase-induced neurotoxicity may result from a prevention or attenuation of oxidative damage induced by glucose oxidase.
Park, Sun-Ji,Kim, Tae-Shin,Park, Choon-Keun,Lee, Sang-Hee,Kim, Jin-Man,Lee, Kyu-Sun,Lee, In-kyu,Park, Jeen-Woo,Lawson, Mark A,Lee, Dong-Seok Society for Endocrinology 2013 Journal of molecular endocrinology Vol.50 No.2
<P>Endoplasmic reticulum (ER) stress generally occurs in secretory cell types. It has been reported that Leydig cells, which produce testosterone in response to human chorionic gonadotropin (hCG), express key steroidogenic enzymes for the regulation of testosterone synthesis. In this study, we analyzed whether hCG induces ER stress via three unfolded protein response (UPR) pathways in mouse Leydig tumor (mLTC-1) cells and the testis. Treatment with hCG induced ER stress in mLTC-1 cells via the ATF6, IRE1a/XBP1, and eIF2α/GADD34/ATF4 UPR pathways, and transient expression of 50 kDa protein activating transcription factor 6 (p50ATF6) reduced the expression level of steroidogenic 3β-hydroxysteroid dehydrogenase △5-△4-isomerase (3β-HSD) enzyme. In an <I>in vivo</I> model, high-level hCG treatment induced expression of p50ATF6 while that of steroidogenic enzymes, especially 3β-HSD, 17α-hydroxylase/C17–20 lyase (CYP17), and 17β-hydrozysteroid dehydrogenase (17β-HSD), was reduced. Expression levels of steroidogenic enzymes were restored by the ER stress inhibitor tauroursodeoxycholic acid (TUDCA). Furthermore, lentivirus-mediated transient expression of p50ATF6 reduced the expression level of 3β-HSD in the testis. Protein expression levels of phospho-JNK, CHOP, and cleaved caspases-12 and -3 as markers of ER stress-mediated apoptosis markedly increased in response to high-level hCG treatment in mLTC-1 cells and the testis. Based on transmission electron microscopy and H&E staining of the testis, it was shown that abnormal ER morphology and destruction of testicular histology induced by high-level hCG treatment were reversed by the addition of TUDCA. These findings suggest that hCG-induced ER stress plays important roles in steroidogenic enzyme expression via modulation of the ATF6 pathway as well as ER stress-mediated apoptosis in Leydig cells.</P>
A Case of Immunoglobulin A Nephropathy in a Patient with Kimura's Disease
Park, Hye Jung,Kim, Jae Kyung,Kim, Hyun Ju,Park, Kwan-Kyu,Bae, Yoon Sung,Lee, Yong Kyu,Kim, Beom Seok Yeungnam University College of Medicine 2013 Yeungnam University Journal of Medicine Vol.30 No.2
Kimura's disease is an angiolymphoid-proliferative disorder that manifests with benign subcutaneous swelling predominantly in the head and the neck. Kidney involvement, including proteinuria, occurs in 12-16% of patients with the disease, and 60-78% of such cases is nephrotic syndrome. Reported etiologies of nephrotic syndrome in Kimura's disease include membranous glomerulonephritis, mesangial proliferative glomerulonephritis, minimal-change disease, focal segmental glomerulosclerosis, diffuse proliferative glomerulonephritis and immunoglobulin A (IgA) nephropathy. There have been only two case reports of IgA nephropathy in Kimura's disease, in 1998. In this report, we present a third case of IgA nephropathy associated with Kimura's disease.