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Articles by E Kim
Total Records ( 8 ) for E Kim
  J. H Kim , K. H Chang , D.G Na , S. H Park , E Kim , D.H Han , H. M Kwon , C. H Sohn and Y.J. Yim
 

BACKGROUND AND PURPOSE: Meningeal inflammatory myofibroblastic tumor (IMT) has been rarely reported, and its prognosis is still unclear. Our purpose was to describe the imaging features of patients with meningeal IMT and their results on follow-up studies.

MATERIALS AND METHODS: Twenty-four MR images in 10 consecutive patients with pathologically proved meningeal IMTs were retrospectively evaluated, focusing on the lesion distribution, signal intensity (SI), and contrast-enhancement pattern with a review of the clinical records.

RESULTS: Eight patients with intracranial IMT showed localized (n = 4) or diffuse (n = 4) dural thickening, a single mass (n = 5) or 2 (n = 2) dural-based masses with surrounding edema, dural venous sinus thrombosis (n = 5), and leptomeningeal involvement (n = 5). Extracranial involvement of the mastoid (n = 2) and orbit (n = 2) was also associated. Each of the 2 patients with intraspinal IMT showed a dural-based mass and a segmental dural thickening, respectively. All of the thickened dura showed low SI on T2-weighted images, iso-SI on T1-weighted images, and diffuse contrast enhancement. Variable recurrences with dural-based masses, mastoid involvement, or nasolacrimal duct involvement were observed in all 4 patients with diffuse intracranial IMT, but not in the others.

CONCLUSIONS: Localized or diffuse dural thickening of T2 low SI and diffuse contrast enhancement combined with dural-based masses are a common MR imaging finding of meningeal intracranial IMT. Adjacent leptomeningeal involvement and dural venous sinus thrombosis are frequently associated. The diffuse type has a tendency toward recurrence.

  B Birmaher , D Axelson , B Goldstein , M Strober , Gill , J Hunt , P Houck , W Ha , S Iyengar , E Kim , S Yen , H Hower , C Esposito Smythers , T Goldstein , N Ryan and M. Keller
 

OBJECTIVE: The authors sought to assess the longitudinal course of youths with bipolar spectrum disorders over a 4-year period. METHOD: At total of 413 youths (ages 7–17 years) with bipolar I disorder (N=244), bipolar II disorder (N=28), and bipolar disorder not otherwise specified (N=141) were enrolled in the study. Symptoms were ascertained retrospectively on average every 9.4 months for 4 years using the Longitudinal Interval Follow-Up Evaluation. Rates and time to recovery and recurrence and week-by-week symptomatic status were analyzed. RESULTS: Approximately 2.5 years after onset of their index episode, 81.5% of the participants had fully recovered, but 1.5 years later 62.5% had a syndromal recurrence, particularly depression. One-third of the participants had one syndromal recurrence, and 30% had two or more. The polarity of the index episode predicted that of subsequent episodes. Participants were symptomatic during 60% of the follow-up period, particularly with subsyndromal symptoms of depression and mixed polarity, with numerous changes in mood polarity. Manic symptomatology, especially syndromal, was less frequent, and bipolar II was mainly manifested by depressive symptoms. Overall, 40% of the participants had syndromal or subsyndromal symptoms during 75% of the follow-up period, and 16% of the participants experienced psychotic symptoms during 17% the follow-up period. Twenty-five percent of youths with bipolar II converted to bipolar I, and 38% of those with bipolar disorder not otherwise specified converted to bipolar I or II. Early onset, diagnosis of bipolar disorder not otherwise specified, long illness duration, low socioeconomic status, and family history of mood disorders were associated with poorer outcomes. CONCLUSIONS: Bipolar spectrum disorders in youths are characterized by episodic illness with subsyndromal and, less frequently, syndromal episodes with mainly depressive and mixed symptoms and rapid mood changes.

  X Wu , M. R Spitz , J. J Lee , S. M Lippman , Y Ye , H Yang , F. R Khuri , E Kim , J Gu , R Lotan and W. K. Hong
 

This study was aimed to identify novel susceptibility variants for second primary tumor (SPT) or recurrence in curatively treated early-stage head and neck squamous cell carcinoma (HNSCC) patients.

We constructed a custom chip containing a comprehensive panel of 9,645 chromosomal and mitochondrial single nucleotide polymorphisms (SNP) representing 998 cancer-related genes selected by a systematic prioritization schema. Using this chip, we genotyped 150 early-stage HNSCC patients with and 300 matched patients without SPT/recurrence from a prospectively conducted randomized trial and assessed the association of these SNPs with risk of SPT/recurrence.

Individually, six chromosomal SNPs and seven mitochondrial SNPs were significantly associated with risk of SPT/recurrence after adjustment for multiple comparisons. A strong gene-dosage effect was observed when these SNPs were combined, as evidenced by a progressively increasing SPT/recurrence risk as the number of unfavorable genotypes increased (P for trend < 1.00 x 10–20). Several polygenic analyses suggest an important role of interconnected functional network and gene-gene interaction in modulating SPT/recurrence. Furthermore, incorporation of these genetic markers into a multivariate model improved significantly the discriminatory ability over the models containing only clinical and epidemiologic variables.

This is the first large-scale systematic evaluation of germ-line genetic variants for their roles in HNSCC SPT/recurrence. The study identified several promising susceptibility loci and showed the cumulative effect of multiple risk loci in HNSCC SPT/recurrence. Furthermore, this study underscores the importance of incorporating germ-line genetic variation data with clinical and risk factor data in constructing prediction models for clinical outcomes.

  J Wang , S. M Lippman , J. J Lee , H Yang , F. R Khuri , E Kim , J Lin , D. W Chang , R Lotan , W. K Hong and X. Wu
 

Curatively treated patients with early-stage head and neck squamous cell carcinoma (HNSCC) are at high risks for second primary tumor (SPT) and recurrence. The regulator of G-protein signaling (RGS) is important in essential signaling transduction and cellular activities. We hypothesize that genetic variations of RGS may modulate the risk of SPT/recurrence in patients with early-stage HNSCC. In a nested case–control study, we evaluated 98 single-nucleotide polymorphisms (SNPs) in 17 RGS genes for the risk of SPT/recurrence among 450 HNSCC patients. Eight SNPs showed significant associations with the risk of SPT/recurrence, with the most significant one of rs2179653, which is located in the 5'-flanking region of RGS2 gene. Under a recessive genetic model, the homozygous variant genotype of this SNP was associated with 2.95-fold [95% confidence interval (CI): 1.52–5.74] increased risk of SPT/recurrence. This association remained significant after the adjustment for multiple comparisons. Cumulative effects analysis revealed that the risk increased significantly with the increasing numbers of unfavorable genotypes. Compared with subjects carrying 0–2 unfavorable genotypes, the hazard ratios (95% CIs) for those carrying 3 or 4+ were 1.73 (1.10–2.70) and 3.05 (1.92–4.83), respectively. Furthermore, survival tree analysis revealed potential higher order gene–gene interactions and indicated different outcomes based on distinct genotype profiles. Genetic variations of RGS genes may modulate the susceptibility to SPT/recurrence in early-stage HNSCC patients individually and cumulatively. Our results stressed the importance of taking a polygenic approach to evaluate the cumulative and interaction effects of genetic variations in the prediction of cancer risk and prognosis.

  X Zhang , H Yang , J. J Lee , E Kim , S. M Lippman , F. R Khuri , M. R Spitz , R Lotan , W. K Hong and X. Wu
 

Second primary tumor (SPT) and/or recurrence negatively impact the prognosis of patients with curatively treated early-stage head and neck cancer. MicroRNAs (miRNAs) play important roles in cancer development. We explored whether the variations of miRNA-related pathway were associated with the risk of SPT/recurrence in patients with early-stage head and neck cancer. This study includes 150 early-stage head and neck cancer patients with SPT/recurrence and 300 patients without SPT/recurrence. Two hundred and thirty-five tagging and potentially functional single-nucleotide polymorphisms (SNPs) were genotyped from eight miRNA biogenesis pathway genes and 135 miRNA-targeted genes. Eighteen miRNA-related SNPs were significantly associated with the risk of SPT/recurrence. The most significant SNP was rs3747238, a miRNA-binding site SNP in SMC1B. The variant homozygous genotype of this SNP was associated with a 1.74-fold increased risk [95% confidence interval (CI) 1.19–2.54; P = 0.004]. Cumulative effect analysis showed joint effects for the number of unfavorable genotype in patients. Survival tree analysis further identified the high-order gene–gene interactions and categorized the study subjects into low-, medium- and high-risk groups. Patients in the high-risk group had a 4.84-fold increased risk (95% CI: 3.11–7.51; P = 2.45 x 10–12) and a shorter event-free median survival time of 37.9 months (log rank P = 2.28 x 10–13). Our results suggested that miRNA-related genetic polymorphisms may be used individually and jointly to predict the risk of SPT/recurrence of early-stage head and neck cancer patients.

  H. J Lee , E Kim and J. S. Kim
 

We present a novel approach for generating targeted deletions of genomic segments in human and other eukaryotic cells using engineered zinc finger nucleases (ZFNs). We found that ZFNs designed to target two different sites in a human chromosome could introduce two concurrent DNA double-strand breaks (DSBs) in the chromosome and give rise to targeted deletions of the genomic segment between the two sites. Using this method in human cells, we were able to delete predetermined genomic DNA segments in the range of several-hundred base pairs (bp) to 15 mega-bp at frequencies of 10–3 to 10–1. These high frequencies allowed us to isolate clonal populations of cells, in which the target chromosomal segments were deleted, by limiting dilution. Sequence analysis revealed that many of the deletion junctions contained small insertions or deletions and microhomologies, indicative of DNA repair via nonhomologous end-joining. Unlike other genome engineering tools such as recombinases and meganucleases, ZFNs do not require preinsertion of target sites into the genome and allow precise manipulation of endogenous genomic scripts in animal and plant cells. Thus, ZFN-induced genomic deletions should be broadly useful as a novel method in biomedical research, biotechnology, and gene therapy.

  T. H Bok , D. G Paeng , E Kim , J Na and D. Kang
 

The acoustic integrated backscattered power (IBP) of the phytoplankton Cochlodinium polykrikoides, which causes red tides in Korean waters, was measured in the laboratory and in the sea in situ to investigate the feasibility of observing red tides using high frequency ultrasound at 5 and 10 MHz. The IBP was measured with cultured C. polykrikoides at abundance levels of 90, 110, 200, 260, 300, 340, 360, 600, 700 and 850 cells/mL in the laboratory. Using the same high frequency acoustic transducers that were attached to the side of a research vessel, the IBP was measured in situ over a 9 km ship track near the Gumo Islands in Yeosu in the Southern Sea of Korea during the red tide season. The IBP was also measured simultaneously with positional information obtained from global positioning system data and by sampling the seawater in which C. polykrikoides was counted to survey the C. polykrikoides distribution in the study area. The IBP in situ was in agreement with that in the laboratory depending on the C. polykrikoides abundance. Consequently, we suggest that it is feasible to use underwater ultrasonic methodology for the observation of red tides in real time in situ.

  H. S Yang , E Kim , S Lee , H. J Park , D. S Cooper , I Rajbhandari and I. Choi
 

To understand the mechanism for ion transport through the sodium/bicarbonate transporter SLC4A4 (NBCe1), we examined amino acid residues, within transmembrane domains, that are conserved among electrogenic Na/HCO3 transporters but are substituted with residues at the corresponding site of all electroneutral Na/HCO3 transporters. Point mutants were constructed and expressed in Xenopus oocytes to assess function using two-electrode voltage clamp. Among the mutants, D555E (charge-conserved substitution of the aspartate at position 555 with a glutamate) produced decreasing HCO3 currents at more positive membrane voltages. Immunohistochemistry showed D555E protein expression in oocyte membranes. D555E induced Na/HCO3-dependent pH recovery from a CO2-induced acidification. Current-voltage relationships revealed that D555E produced an outwardly rectifying current in the nominally CO2/HCO3-free solution that was abolished by Cl removal from the bath. In the presence of CO2/HCO3, however, the outward current produced by D555E decreased only slightly after Cl removal. Starting from a Cl-free condition, D555E produced dose-dependent outward currents in response to a series of chloride additions. The D555E-mediated chloride current decreased by 70% in the presence of CO2/HCO3. The substitution of Asp555 with an asparagine also produced a Cl current. Anion selectivity experiments revealed that D555E was broadly permissive to other anions including NO3. Fluorescence measurements of chloride transport were done with human embryonic kidney HEK 293 cells expressing NBCe1 and D555E. A marked increase in chloride transport was detected in cells expressing D555E. We conclude that Asp555 plays a role in HCO3 selectivity.

 
 
 
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