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Regional Variations of Cellular Slime Molds Referred to Ribosomal DNA
홍영빈,강경미,장남기 한국생태학회 2001 Journal of Ecology and Environment Vol.24 No.6
Regional variations of Dictyostelid cellular slime molds were examined using molecular data. The intertranscribed spacer regions including the 5.8S ribosomal DNA of 2 species(D. purpureum, P. violaceum) of Cellular Slime Molds were sequenced and analyzed. Among 13 strains of D. purpureum and 12 strains of P. violaceum analyzed, each two strains were obtained from ATCC and the others were isolated from the forest soils in Korea. The sequences of the 5.8S ribosomal DNA were conserved among the strains of the same species, but unexpectedly highly variable among species. A high level of genetic diversity was found which was best resolved at the genus/species level as well as the family level by sequence data from the ITS 1 and ITS 2 regions. According to the sequence alignments by CLUSTAL X and the phylogeographic analyses by PAUP, 12 strains of P. violaceum were divided into three groups among which there were no difference of the morphological characteristics. Among 13 strains of D. purpureum, genetic variations were related to two morphological types, the temperate and subtropical type. There was no variation pattern according to geography in Korea, but there were some variations between Korea and other countries.
Dynamic Transcriptional Events in Distal Sural Nerve Revealed by Transcriptome Analysis
홍영빈,최병옥,정성철,이진호,문희수,정기화 한국뇌신경과학회 2014 Experimental Neurobiology Vol.23 No.2
Compared with biochemical information available about the diseases in the central nervous system, that for peripheral neuropathyis quite limited primarily due to the difficulties in obtaining samples. Characterization of the core pathology is a prerequisite to thedevelopment of personalized medicine for genetically heterogeneous diseases, such as hereditary motor and sensory neuropathy(HMSN). Here, we first documented the transcriptome profile of distal sural nerve obtained from HMSN patients. RNA-seqanalysis revealed that over 12,000 genes are expressed in distal sural nerve. Among them 4,000 transcripts are novel and 10 fusiongenes per sample were observed. Comparing dataset from whole exome sequencing revealed that over 1,500 transcriptional basemodifications occur during transcription. These data implicate that dynamic alterations are generated when genetic informationare transitioned in distal sural nerve. Although, we could not find significant alterations associated with HMSN, these data mightprovide crucial information about the pathophysiology of HMSN. Therefore, next step in the development of therapeutic strategyfor HMSN might be unveiling biochemical and biophysical abnormalities derived from those potent variation.
Inhibition of cell proliferation by a resveratrol analog in human pancreatic and breast cancer cells
홍영빈,Hyo Jin Kang,Hee Jeong Kim,Eliot M. Rosen,Sivanesan Dakshanamurthy,Riccardo Rondanin,Riccardo Baruchello,Giuseppina Grisolia,Simoni Daniele,배인수 생화학분자생물학회 2009 Experimental and molecular medicine Vol.41 No.3
Resveratrol has been reported to possess cancer preventive properties. In this study, we analyzed anti-tumor activity of a newly synthesized resveratrol analog, cis-3,4',5-trimethoxy-3'-hydroxystilbene (hereafter called 11b) towards breast and pancreatic cancer cell lines. 11b treatments reduced the proliferation of human pancreatic and breast cancer cells, arrested cells in the G2/M phase, and increased the percentage of cells in the subG1/G0 fraction. The 11b treatments also increased the total levels of mitotic checkpoint proteins such as BubR1, Aurora B, Cyclin B, and phosphorylated histone H3. Mechanistically, 11b blocks microtubule polymerization in vitro and it disturbed microtubule networks in both pancreatic and breast cancer cell lines. Computational modeling of the 11b-tubulin interaction indicates that the dimethoxyphenyl group of 11b can bind to the colchicine binding site of tubulin. Our studies show that the 11b treatment effects occur at lower concentrations than similar effects associated with resveratrol treatments and that microtubules may be the primary target for the observed effects of 11b. These studies suggest that 11b should be further examined as a potentially potent clinical chemotherapeutic agent for treating pancreatic and breast cancer patients.
박진모,홍영빈,정기화,최병옥 대한근전도전기진단의학회 2013 대한근전도 전기진단의학회지 Vol.15 No.1
Objectives: Hereditary peripheral neuropathy (HPN) is the most common inherited neuropathy and a genetically and clinically heterogeneous disorder. HPN consists of hereditary motor and sensory neuropathy [HMSN, also called as Charcot-Marie-Tooth disease (CMT)], distal hereditary motor neuropathy (dHMN), hereditary sensory neuropathy (HSN), and hereditary neuropathy with a liability to pressure palsy (HNPP). More than 60 genes have been identified as HPN causative genes. Methods: We analyzed genetic causes from 581 Korean inherited peripheral neuropathy families to determine the frequencies according to each subtype or genetic cause within this clinic population. Results: We identified 18 causative CMT genes (BSCL2, EGR2, GARS, GDAP1, GJB1, HSPB1, HSPB8, MFN2, MPZ, MYH14, NEFL, PMP22, PRPS1, PRX, SBF1, SPTLC1, TFG, and TUBB3) from 316 unrelated families (54.5%). The most frequent genetic cause was PMP22 duplication/deletion, which causes CMT1A/HNPP, and the next is GJB1 mutation causing CMTX1. Conclusion: Although genetic causes have not been determined in many cases, this study revealed that genetic background of HPN in Koreans is considerablely different from other ethnic groups. This study will be useful for development of exact molecular diagnostic tools for HPN.
김은영,홍영빈,고상희,Beobyi Lee,정성철 생화학분자생물학회 2006 Experimental and molecular medicine Vol.38 No.4
disease caused by deficiency of glucocerebro-sidase, resulting in the accumulation of glu-cosylceramide in lysosomes. The neuronopathic forms of this disease are associated with neuronal loss and neurodegeneration. However, the patho-physiological mechanisms leading to prenatal and neonatal death remain uncharacterized. To in-vestigate brain dysfunction in Gaucher disease, we studied the effects of neurotrophic factors during development in a mouse model of Gaucher disease. The expression of brain-derived neurotrophic factor and nerve growth factor was reduced in the cerebral cortex, brainstem, and cerebellum of Gaucher mice, compared with that in wild-type mice. Extracellular signal-regulated kinase (ERK) 1/2 expression was downregulated in neurons from Gaucher mice and correlated with a decreased number of neurons. trophic factors could be involved in neuronal loss in Gaucher disease.
강경미,홍영빈,이재봉,장남기 한국생태학회 1998 Journal of Ecology and Environment Vol.21 No.5
In this study, the occurrence and distribution of dictyostelid cellular slime molds was investigted from soils of typical forests in Mt. Nam and the effect of soil environmental factor on cellular slime molds was investigated. The fourteen species including two undescribed species were isolated as follows: Dictyostelium brefeldianum, Polysphondylium pallidum, P. violaceum, P. pseudo-candidum in Quercus mongolica-Sorbus alnifolia forests, D. purpureum, D. mucoroides var. stoloniferum, D. dimigraformum, D. brefeldiamum, P. pallidum, P. tenuissimum, P. violoceum, P. candidum, P. pseudo-candidum in Pinus densiflora forests, D. polycephahum, D. capitatum, d. brefeldianun, P. candidum in Robinia pseudo-acacia forests, D. purpureum, D. aureostipes var, aureostipes, D. polycephalum in Quercus acutissima forests, D. minutum, D. implicatum. in the site disturbed by human. The dominant species were P. pallidum, D. brefeldiamum, P. pseudo-candidum and D. dimigraformum were the undescribed species in Korea. Environmental factors such as soil pH, water content, organic content, total nitrogen and total phosphorus made a little effect on total species number, the number of clones.
Ultrasonography-guided transplantation facilitates perineural delivery of stem cells
김상범,주재순,홍영빈,최병옥 한국통합생물학회 2015 Animal cells and systems Vol.19 No.4
Treatment options for peripheral neuropathy are very limited. In order to develop a therapeutic strategy using stem cell therapy for the peripheral nervous system, we explored the feasibility of a new delivery method. Using ultrasonographyguided transplantation, human mesenchymal stem cells (hMSCs) were delivered into the perineural region of small rodent models. An optical imaging system revealed that hMSCs stained with CFSE or PKH26 reside for a week posttransplantation in both the mouse and rat. Immunofluorescence analysis of tissues revealed the presence of transplanted hMSCs in the perineural region of mice. At the end of the experiments, no behavioral or phenotypic abnormalities were observed. In addition, H&E and toluidine blue staining showed the integrity of the sciatic nerve after transplantation. This is the first study, to the best of our knowledge, to deliver cells into the perineural region under ultrasonography guidance. Since hMSCs can reside for a considerable time at a transplanted site, an anti-inflammatory efficacy of the transplanted hMSCs can be expected in the perineural region. In conclusion, we established a new administration route for inflammatory peripheral neuropathy without complications, and this may be used for delivery of chemical drugs or stem cells.
Novel Compound Heterozygous Nonsense PRX Mutations in a Korean Dejerine-Sottas Neuropathy Family
최예지,현영세,남수현,구혜수,홍영빈,정기화,최병옥 대한신경과학회 2015 Journal of Clinical Neurology Vol.11 No.1
Background Mutations in the gene encoding periaxin (PRX) are known to cause autosomalrecessive Dejerine-Sottas neuropathy (DSN) or Charcot-Marie-Tooth disease type 4F. However, there have been no reports describing Korean patients with these mutations. Case Report We examined a Korean DSN patient with an early-onset, slowly progressive,demyelinating neuropathy with prominent sensory involvement. Whole-exome sequencing andsubsequent capillary sequencing revealed novel compound heterozygous nonsense mutations(p.R392X and p.R679X) in PRX. One mutation was transmitted from each of the patient’s parents. No unaffected family member had both mutations, and the mutations were not found inhealthy controls. Conclusions We believe that these novel compound heterozygous nonsense mutations arethe underlying cause of DSN. The clinical, electrophysiologic, and pathologic phenotypes inthis family were similar to those described previously for patients with PRX mutations. Wehave identified the first PRX mutation in a Korean patient with DSN.