• Title/Summary/Keyword: Aberrant

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Compression Neuropathy (압박성 신경병증)

  • Kim, Byung-Sung
    • The Journal of Korean Orthopaedic Ultrasound Society
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    • v.1 no.2
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    • pp.128-133
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    • 2008
  • Nerve compression is caused by external force or internal pathology, which symptom develops along nerve distribution. There are median, ulnar and radial nerve compression neuropathies below elbow. Carpal tunnel syndrome at the flexor retinaculum is most common among all the entrapment neuropathies. Other causes of median nerve neuropathy include Struther's ligament, biceps aponeurosis, pronator teres, FDS aponeurosis and aberrant muscles, which induce pronator syndrome or anterior interosseous nerve syndrome. Ulnar nerve can be compressed at the elbow by arcade of Struther, medial epicondylar groove, FCU two heads, which develops cubital tunnel syndrome, at the wrist by ganglion, fracture of hamate hook and vascular problem, which develops Guyon's canal syndrome. Radial tunnel syndrome is caused by supinator muscle, which compresses its deep branch. Treatment is conservative at initial stage like NSAID, night splint or steroid injection. If symptom persists, operative treatment should be considered after electrodiagnostic or imaging studies.

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MicroRNA Regulation in Systemic Lupus Erythematosus Pathogenesis

  • Yan, Sheng;Yim, Lok Yan;Lu, Liwei;Lau, Chak Sing;Chan, Vera Sau-Fong
    • IMMUNE NETWORK
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    • v.14 no.3
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    • pp.138-148
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    • 2014
  • MicroRNAs (miRNAs) are endogenous small RNA molecules best known for their function in post-transcriptional gene regulation. Immunologically, miRNA regulates the differentiation and function of immune cells and its malfunction contributes to the development of various autoimmune diseases including systemic lupus erythematosus (SLE). Over the last decade, accumulating researches provide evidence for the connection between dysregulated miRNA network and autoimmunity. Interruption of miRNA biogenesis machinery contributes to the abnormal T and B cell development and particularly a reduced suppressive function of regulatory T cells, leading to systemic autoimmune diseases. Additionally, multiple factors under autoimmune conditions interfere with miRNA generation via key miRNA processing enzymes, thus further skewing the miRNA expression profile. Indeed, several independent miRNA profiling studies reported significant differences between SLE patients and healthy controls. Despite the lack of a consistent expression pattern on individual dysregulated miRNAs in SLE among these studies, the aberrant expression of distinct groups of miRNAs causes overlapping functional outcomes including perturbed type I interferon signalling cascade, DNA hypomethylation and hyperactivation of T and B cells. The impact of specific miRNA-mediated regulation on function of major immune cells in lupus is also discussed. Although research on the clinical application of miRNAs is still immature, through an integrated approach with advances in next generation sequencing, novel tools in bioinformatics database analysis and new in vitro and in vivo models for functional evaluation, the diagnostic and therapeutic potentials of miRNAs may bring to fruition in the future.

DNA METHYLATION OF TPEF GENE IN HEAD AND NECK SQUAMOUS CELL CARCINOMA CELL LINES (두경부암 세포주에서 TPEF 유전자의 methylation 변이)

  • Chun, So-Young;Kim, Jung-Ock;Hong, Su-Hyung;Chung, Yu-Kyung;Jang, Hyun-Jung;Shon, Yoon-Kyung;Kim, Jung-Wan
    • Journal of the Korean Association of Oral and Maxillofacial Surgeons
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    • v.31 no.6
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    • pp.468-473
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    • 2005
  • Head and neck squamous cell carcinoma (HNSCC) is the sixth most common malignancy worldwide. The molecular mechanisms involved in the development and progression of these carcinomas are not well known. Abnormalities of genomic methylation patterns have been attributed a role in carcinogenesis and local de novo methylation at tumor suppressor loci was held to be involved in silencing of tumor suppressor genes. Using Ms APPCR, we previously isolated a hypermethylated fragment corresponded to the 5' end of TPEF gene from primary liver and lung cancer cells. To confirm the inactivation of TPEF gene by hypermethylation in HNSCC, we investigated correlation between methylation pattern and expression of TPEF in 10 HNSCC cell lines. In methylation analysis such as combined-bisulfite restriction analysis(COBRA) and bisulfite sequencing, only RPMI 2650 showed none methylated pattern and another 9 cell lines showed dense methylation. The TPEF gene expression level analysis using RT-PCR showed that these 9 cell lines had not or significantly low expression levels of TPEF as compared with RPMI 2650. In addition, the increase of TPEF reexpression by 5-AzaC as demethylating agent in 9 cell lines also indicated that TPEF expression was regulated by hypermethylation. These results of this study demonstrate that epigenetic silencing of TPEF gene by aberrant methylation could play an important role in HNSCC carcinogenesis.

The Effect of Over-expression and Inactivation of Nuclear Factor I-C on the Dentin Matrix Gene Expression of MDPC-23 Odontoblasts (Nuclear Factor I-C 과발현과 발현억제가 MDPC-23 상아모세포주의 상아질 기질유전자 발현에 미치는 영향)

  • Bae, Hyun-Sook;Cho, Young-Sik
    • Journal of dental hygiene science
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    • v.9 no.4
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    • pp.427-433
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    • 2009
  • Nuclear factor I-C (NFI-C) null mice demonstrated aberrant odontoblast differentiation and abnormal dentin formation. In order to elucidate the mechanisms responsible for these changes, we evaluated the expression of dentin matrix gene after over-expression and inactivation of NFI-C in MDPC-23 cells by reverse transcription-polymerase chain reaction (RT-PCR) analysis. Collagen type I (Col I), osteocalcin (OC), and dentin sialophosphoprotein (DSPP) expression was decreased after inactivation of NFI-C. However, bone sialoprotein (BSP) expression was dramatically increased after inactivation of NFI-C. ALP and DMP4 expression was not changed after inactivation of NFI-C. The expression of alkaline phoshatase (ALP) and dentin matrix protein 4 (DMP4) was increased after over-expression of NFI-C, while Col I, OC, DSPP, and BSP expression was decreased. These findings suggest that odontoblasts after loss of NFI-C lost the phenotype of odontoblasts and acquired those of osteoblasts.

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A Case of Pleural Effusion after Malposition of Central Venous Catheter (중심정맥카테터 삽입의 이상위치로 발생한 편측성 흉수 1례)

  • Kim, Jae Seok;Kim, Sang-Ha;Lee, Nak Won;Kwon, Woo Cheol;Choi, Hun;Beon, Jong Won;Hong, Tae Won;Shin, Kye Chul;Yong, Suk Joong
    • Tuberculosis and Respiratory Diseases
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    • v.60 no.6
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    • pp.690-693
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    • 2006
  • Central venous catheterization is used to provide a large amount of fluid, total parenteral nutrition and to administer antitumor agents with few complications reported. We report an uncommon case of pleural effusion that occurred after central venous catheterization. In many cases, the mechanism for the pleural effusion after central venous catheterization occurs through an injury to the superior vena cava by the continuous mechanical force of the catheter tip, the flow of large amount of fluid and an osmotic injury to the wall of the vein. This case is somewhat different in that the central catheter was placed in an aberrant vessel resulting in the pleural effusion. A post-placement chest roentgenogram and the correct approach of catheterization are important for preventing this complication.

Changes in gene expression associated with oocyte meiosis after $Obox4$ RNAi

  • Lee, Hyun-Seo;Kim, Eun-Young;Lee, Kyung-Ah
    • Clinical and Experimental Reproductive Medicine
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    • v.38 no.2
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    • pp.68-74
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    • 2011
  • Objective: Previously, we found that oocyte specific homeobox (Obox) 4 plays significant role in completion of meiosis specifically at meiosis I-meiosis II (MI-MII) transition. The purpose of this study was to determine the mechanism of action of $Obox4$ in oocyte maturation by evaluating downstream signal networking. Methods: The $Obox4$ dsRNA was prepared by $in$ $vitro$ transcription and microinjected into the cytoplasm of germinal vesicle oocytes followed by $in$ $vitro$ maturation in the presence or absence of 0.2 mM 3-isobutyl-1-metyl-xanthine. Total RNA was extracted from 200 oocytes of each group using a PicoPure RNA isolation kit then amplified two-rounds. The probe hybridization and data analysis were used by Affymetrix Gene-Chip$^{(R)}$ Mouse Genome 430 2.0 array and GenPlex 3.0 (ISTECH, Korea) software, respectively. Results: Total 424 genes were up (n=80) and down (n=344) regulated after $Obox4$ RNA interference (RNAi). Genes mainly related to metabolic pathways and mitogen-activated protein kinase (MAPK) signaling pathway was changed. Among the protein kinase C (PKC) isoforms, PKC-alpha, beta, gamma were down-regulated and especially the MAPK signaling pathway PKC-gamma was dramatically decreased by $Obox4$ RNAi. In the cell cycle pathway, we evaluated the expression of genes involved in regulation of chromosome separation, and found that these genes were down-regulated. It may cause the aberrant chromosome segregation during MI-MII transition. Conclusion: From the results of this study, it is concluded that $Obox4$ is important upstream regulator of the PKC and anaphase-promoting complex action for maintaining intact germinal vesicle.

Genetic variation of 7S and 11S globulins in soybean seed (콩 종실 단백질의 유전변이)

    • Korean Journal of Plant Resources
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    • v.12 no.3
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    • pp.198-203
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    • 1999
  • 7S and 11S globulins are two major storage proteins in soybean seed. For improving the quality of soybean seed protein, an increase of 11S/7S ratio would be a desirable objective because 11S globulin contains much more sulfur-containing amino acids than 7S globulin. In this study, six soybean varieties grown at three locations were used for genetic variation analysis of 7S and 11S globulins. It was possible to screen the soybean genotypes having aberrant subunit compositions of the two globulins by a sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE). So, heritabilities, genotypic and phenotypic correlations among eight globulin fraction contents of soybean seeds were estimated. The mean value of 7S and 11S globulin fraction contents were 38.9% and 61.1%, respectively, and the ratio of 7S to 11S globulin ranged from 0.58 to 0.74. The high heritability value was found in $\beta$ subunits but the values of acidic and basic subunits were relatively low. Genotypic correlations were higher than the corresponding phenotypic correlations in most of globulin subunit contents. $\beta$ subunits was negatively correlated with $\alpha$ and $\alpha$' subunits among 7S fractions, while no significant correlation between $\alpha$ and $\alpha$' subunits could be found In case of 11S fractions, acidic and basic subunits exhibited no genotypic but negative phenotypic correlation.

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Long Non-Coding RNA CCAT1 Acts as a Competing Endogenous RNA to Regulate Cell Growth and Differentiation in Acute Myeloid Leukemia

  • Chen, Lianxiang;Wang, Wei;Cao, Lixia;Li, Zhijun;Wang, Xing
    • Molecules and Cells
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    • v.39 no.4
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    • pp.330-336
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    • 2016
  • Long non-coding RNAs (lncRNAs) are involved in multiple cellular events, as well as in tumorigenesis. Colon cance-rassociated transcript-1 (CCAT1) gene encodes an lncRNA whose over-activation was observed in an expanding list of primary human solid tumors and tumor cell lines, however its biological roles in acute myeloid leukaemia (AML) has not been reported yet at present. In this study, the aberrant upregulation of CCAT1 was detected in French-American-British M4 and M5 subtypes of adult AML patients. By gain- and loss-of-function analysis, we determined that CCAT1 repressed monocytic differentiation and promoted cell growth of HL-60 by sequestering tumor suppressive miR-155. Accordingly, a significant decrease in miR-155 level was detected in AML patients. Reintroduction of miR-155 into HL-60 cells restored monocytic maturation and repressed cell proliferation. Furthermore, CCAT1 could up-regulated c-Myc via its competing endogenous RNA (ceRNA) activity on miR-155. In conclusion, these results revealed new mechanism of lncRNA CCAT1 in AML development, and suggested that the manipulation of CCAT1 expression could serve as a potential strategy in AML therapy.

Physiological Functions of the COPI Complex in Higher Plants

  • Ahn, Hee-Kyung;Kang, Yong Won;Lim, Hye Min;Hwang, Inhwan;Pai, Hyun-Sook
    • Molecules and Cells
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    • v.38 no.10
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    • pp.866-875
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    • 2015
  • COPI vesicles are essential to the retrograde transport of proteins in the early secretory pathway. The COPI coatomer complex consists of seven subunits, termed ${\alpha}-$, ${\beta}-$, ${\beta}^{\prime}-$, ${\gamma}-$, ${\delta}-$, ${\varepsilon}-$, and ${\zeta}$-COP, in yeast and mammals. Plant genomes have homologs of these subunits, but the essentiality of their cellular functions has hampered the functional characterization of the subunit genes in plants. Here we have employed virus-induced gene silencing (VIGS) and dexamethasone (DEX)-inducible RNAi of the COPI subunit genes to study the in vivo functions of the COPI coatomer complex in plants. The ${\beta}^{\prime}-$, ${\gamma}-$, and ${\delta}$-COP subunits localized to the Golgi as GFP-fusion proteins and interacted with each other in the Golgi. Silencing of ${\beta}^{\prime}-$, ${\gamma}-$, and ${\delta}$-COP by VIGS resulted in growth arrest and acute plant death in Nicotiana benthamiana, with the affected leaf cells exhibiting morphological markers of programmed cell death. Depletion of the COPI subunits resulted in disruption of the Golgi structure and accumulation of autolysosome-like structures in earlier stages of gene silencing. In tobacco BY-2 cells, DEX-inducible RNAi of ${\beta}^{\prime}$-COP caused aberrant cell plate formation during cytokinesis. Collectively, these results suggest that COPI vesicles are essential to plant growth and survival by maintaining the Golgi apparatus and modulating cell plate formation.

A Case of Pulmonary Sequestration Infected by $Mycobacterium$ $tuberculosis$ (폐결핵이 동반된 폐격리증 1예)

  • Shin, Ji-Young;Park, Hee-Sun;Yoo, Su-Jin;Jung, Sun-Young;Park, Ji-Won;Kim, Ju-Ock;Kim, Sun-Young;Lee, Jeong-Eun
    • Tuberculosis and Respiratory Diseases
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    • v.70 no.1
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    • pp.79-83
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    • 2011
  • Pulmonary sequestration is a rare anomaly, in which a local area of a lung is supplied separately by an anomalous artery that arises from the aorta or one of its branches. Infection, mainly bacterial, is a major complication of sequestration. We report the case of a 17-year-old male patient, who presented with cough and fever. The contrast-enhanced chest computer tomomgraphy (CT) scans revealed an aberrant artery that originated from the descending thoracic aorta. He underwent a left-lower lobectomy. Macroscopically, the abnormal segment presented as multiple heterogenous cystic and solid lesions, and the cysts were filled with mucoid and pus-like material. Histology showed that the pulmonary parenchyma had been replaced by caseating epitheloid granulomas. The mycobacterial culture of his sputum was positive. On the basis of these results, the diagnosis of tuberculosis was established. The patient was treated with anti-tuberculous medication for 6 months, and 1 year later, his clinical status remained excellent.