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Articles by M. J Kim
Total Records ( 5 ) for M. J Kim
  S. H Kim , J Lee , M. J Kim , Y. H Jeon , Y Park , D Choi , W. J Lee and H. K. Lim
 

OBJECTIVE. We compared the diagnostic performance of gadoxetic acid–enhanced MRI with that of triple-phase 16-, 40-, and 64-MDCT in the preoperative detection of hepatocellular carcinoma (HCC).

SUBJECTS AND METHODS. Sixty-two consecutively registered patients (54 men, eight women; age range, 31–67 years) with 83 HCCs underwent triple-phase (arterial, portal venous, equilibrium) CT at 16-, 40-, or 64-MDCT and gadoxetic acid–enhanced 3-T MRI. The diagnosis of HCC was established after surgical resection. Three observers independently and randomly reviewed the MR and CT images on a tumor-by-tumor basis. The diagnostic accuracy of these techniques in the detection of HCC was assessed with alternative free response receiver operating characteristic (ROC) analysis. Sensitivity, positive and negative predictive values, and sensitivity according to tumor size were evaluated.

RESULTS. For each observer, the areas under the ROC curve were 0.971, 0.959, and 0.967 for MRI and 0.947, 0.950, and 0.943 for CT. The differences were not statistically significant between the two techniques for each observer (p > 0.05). The differences in sensitivity and positive and negative predictive values between the two techniques for each observer were not statistically significant (p > 0.05). Among 10 HCCs 1 cm in diameter or smaller, each of the observers detected seven tumors with MRI. With CT, one observer detected five, one observer detected four, and one observer detected three HCCs with no statistically significant difference (p > 0.05).

CONCLUSION. Gadoxetic acid–enhanced MRI and triple-phase MDCT have similar diagnostic performance in the preoperative detection of HCC, but MRI may be better than MDCT in the detection of HCC 1 cm in diameter or smaller.

  J. Y Choi , M. J Kim , J. Y Lee , J. S Lim , J. J Chung , K. W Kim and H. S. Yoo
 

OBJECTIVE. The purpose of this article is to present the typical and atypical manifestations of serous cystadenoma, which can be visualized with cross-sectional imaging.

CONCLUSION. Serous cystadenomas of the pancreas have various distinguishing imaging features. Typically, a serous cystadenoma is morphologically classified as having either a polycystic, honeycomb, or oligocystic pattern. Atypical manifestations of serous cystadenoma can include giant tumors with ductal dilatation, intratumoral hemorrhages, solid variants, unilocular cystic tumors, interval growth, and a disseminated form.

  A Kim , M. J Kim , Y Yang , J. W Kim , Y. I Yeom and J. S. Lim
 

Downregulation of the N-myc downstream-regulated gene 2 (NDRG2) gene is involved in the progression of aggressive forms of cancer, along with the poor prognosis of cancer patients. In the current study, we examined the effect of NDRG2 expression on the metastatic potential of HT1080 human fibrosarcoma and B16F10 murine melanoma cells in both in vitro and in vivo systems. In gelatin zymography, NDRG2 expression remarkably suppressed the matrix metalloproteinase (MMP)-9 activity and slightly inhibited MMP-2 activity of both cell lines. Tumor migration and invasion in vitro were significantly reduced by NDRG2 expression, and NDRG2 inhibited tumor cell proliferation in an anchorage-independent semisolid agar assay. Specifically, we found that NDRG2 affects invasion through suppression of nuclear factor kappa B (NF-B) activity. In animal experiments, subcutaneously injected B16F10-NDRG2 cells showed delayed tumor growth compared with B16F10-mock cells. Furthermore, severe metastasis from primary tumor mass into the draining lymph nodes was observed after injection of B16F10-mock cells, but not with B16F10-NDRG2 cells. Pulmonary metastasis after intravenous injection of B16F10 cells was also reduced by NDRG2 expression. Intra- and peritumoral angiogenesis that is critical for the tumor growth and metastasis was clearly found in tumors after injection with B16F10-mock cells, whereas it was impaired in tumors after injection with B16F10-NDRG2 cells. Collectively, our data show that NDRG2 expression significantly suppresses tumor invasion by inhibiting MMP activities, which are regulated through the NF-B signaling. Moreover, results from animal experiments provide evidence for the regulatory role of the NDRG2 gene in metastatic tumors.

  J. Y Byun , C. H Yoon , S An , I. C Park , C. M Kang , M. J Kim and S. J. Lee
 

To prevent the development of malignancies, mammalian cells activate disposal programs, such as programmed cell death, in response to deregulated oncogene expression. However, the molecular basis for regulation of cellular disposal machinery in response to activated oncogenes is unclear at present. In this study, we show that upregulation of the autophagy-related protein, Atg5, is critically required for the oncogenic H-ras-induced autophagic cell death and that Rac1/mitogen-activated kinase kinase (MKK) 7/c-Jun N-terminal kinase (JNK) signals upregulation of Atg5. Overexpression of H-rasV12 induced marked autophagic vacuole formation and cell death in normal fibroblasts, which remained unaffected by a caspase inhibitor. Pretreatment with Bafilomycin A1, an autophagy inhibitor, completely attenuated H-rasV12-induced cell death as well as autophagic vacuole formation. Selective production of Atg5 was observed in cells overexpressing H-rasV12, and small interfering RNA (siRNA) targeting of Atg5 clearly inhibited autophagic cell death. Interestingly, inhibition of JNK or c-Jun by specific siRNA suppressed Atg5 upregulation and autophagic cell death. Moreover, inhibition of MKK7, but not MKK4, effectively attenuated H-rasV12-induced JNK activation. In addition, ectopic expression of RacN17 or Rac1-siRNA effectively inhibited MKK7–JNK activation, Atg5 upregulation and autophagic cell death. These data support the notion that upregulation of Atg5 is required for the oncogenic H-ras-induced autophagic cell death in normal fibroblasts and that activation of Rac1/MKK7/JNK-signaling pathway leads to upregulation of Atg5 in response to oncogenic H-ras. Our findings suggest that in cells acquiring deregulated oncogene expression, oncogenic stress triggers autophagic cell death, which protects cells against malignant progression.

  M. J Kim , S Ciani and D. P. Schachtman
 

Reactive oxygen species (ROS) play an important role in root responses to potassium deprivation by regulating the expression of the high-affinity K+ transporter gene AtHAK5 and other genes. Activation-tagged lines of Arabidopsis plants containing the AtHAK5 promoter driving luciferase were screened for bioluminescence under potassium-sufficient conditions. A member of the type III peroxidase family, RCI3, was isolated and when it was overexpressed by the activation tag, this led to the enhanced expression of luciferase and the endogenous AtHAK5. RCI3 was found to be up-regulated upon potassium deprivation. Plants overexpressing RCI3 (RCI3-ox) showed more ROS production and AtHAK5 expression whereas the ROS production and AtHAK5 expression were reduced in rci3-1 under K+-deprived conditions. These results suggested that RCI3 is involved in the production of ROS under potassium deprivation and that RCI3-mediated ROS production affects the regulation of AtHAK5 expression. This peroxidase appears to be another component of the low-potassium signal transduction pathway in Arabidopsis roots.

 
 
 
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