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Articles by J Lee
Total Records ( 15 ) for J Lee
  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.

  M. F Green , J Lee , M. S Cohen , S. A Engel , A. S Korb , K. H Nuechterlein , J. K Wynn and D. C. Glahn
 

Context  Visual masking procedures assess the earliest stages of visual processing. Patients with schizophrenia reliably show deficits on visual masking, and these procedures have been used to explore vulnerability to schizophrenia, probe underlying neural circuits, and help explain functional outcome.

Objective  To identify and compare regional brain activity associated with one form of visual masking (ie, backward masking) in schizophrenic patients and healthy controls.

Design  Subjects received functional magnetic resonance imaging scans. While in the scanner, subjects performed a backward masking task and were given 3 functional localizer activation scans to identify early visual processing regions of interest (ROIs).

Setting  University of California, Los Angeles, and the Department of Veterans Affairs Greater Los Angeles Healthcare System.

Participants  Nineteen patients with schizophrenia and 19 healthy control subjects.

Main Outcome Measure  The magnitude of the functional magnetic resonance imaging signal during backward masking.

Results  Two ROIs (lateral occipital complex [LO] and the human motion selective cortex [hMT+]) showed sensitivity to the effects of masking, meaning that signal in these areas increased as the target became more visible. Patients had lower activation than controls in LO across all levels of visibility but did not differ in other visual processing ROIs. Using whole-brain analyses, we also identified areas outside the ROIs that were sensitive to masking effects (including bilateral inferior parietal lobe and thalamus), but groups did not differ in signal magnitude in these areas.

Conclusions  The study results support a key role in LO for visual masking, consistent with previous studies in healthy controls. The current results indicate that patients fail to activate LO to the same extent as controls during visual processing regardless of stimulus visibility, suggesting a neural basis for the visual masking deficit, and possibly other visual integration deficits, in schizophrenia.

  B. Y Park , C. W Jeong , E. A Jang , S. J Kim , S. T Jeong , M. H Shin , J Lee and K. Y. Yoo
  Background

The optimal dose of remifentanil to attenuate the cardiovascular responses to tracheal intubation in pre-eclamptic patients undergoing Caesarean delivery under general anaesthesia has not been established. We compared the effects of two low doses of remifentanil on the cardiovascular responses to tracheal intubation and neonatal outcomes.

Methods

Forty-eight women with severe pre-eclampsia were randomly assigned to receive either remifentanil 0.5 µg kg–1 (R0.5 group, n=24) or 1 µg kg–1 (R1.0 group, n=24) over 30 s before induction of anaesthesia using thiopental 5 mg kg–1 and succinylcholine 1.5 mg kg–1. Systolic arterial pressure (SAP), heart rate (HR), and plasma catecholamine concentrations were measured. Neonatal effects were assessed using Apgar scores and umbilical cord blood gas analysis.

Results

SAP was decreased by induction of anaesthesia and increased by tracheal intubation in both groups. The peak SAP after intubation was greater in the R0.5 group than in the R1.0 group, whereas it did not exceed baseline values in either group. HR increased significantly above baseline in both groups with no significant differences between the groups. Three subjects in the R1.0 group received ephedrine due to hypotension (SAP<90 mm Hg). Norepinephrine concentrations remained unaltered after intubation and increased significantly at delivery with no significant differences between the groups. Neonatal Apgar scores and umbilical arterial and venous pH and blood gas values were comparable between the groups.

Conclusions

Both doses of remifentanil effectively attenuated haemodynamic responses to tracheal intubation with transient neonatal respiratory depression in pre-eclamptic patients undergoing Caesarean delivery under general anaesthesia. The 1.0 µg kg–1 dose was associated with hypotension in three of 24 subjects.

  J Lee , E. R Hahm and S. V. Singh
 

We have shown previously that withaferin A (WA), a promising anticancer constituent of Ayurvedic medicine plant Withania somnifera, inhibits growth of human breast cancer cells in culture and in vivo in association with apoptosis induction. The present study builds on these observations and demonstrates that WA inhibits constitutive as well as interleukin-6 (IL-6)-inducible activation of signal transducer and activator of transcription 3 (STAT3), which is an oncogenic transcription factor activated in many human malignancies including breast cancer. The WA treatment (2 and 4 µM) decreased constitutive (MDA-MB-231) and/or IL-6-inducible (MDA-MB-231 and MCF-7) phosphorylation of STAT3 (Tyr705) and its upstream regulator Janus-activated kinase 2 (JAK2; Tyr1007/1008) in MDA-MB-231, which was accompanied by suppression of their protein levels especially at the higher concentration. Exposure of MDA-MB-231 or MCF-7 cells to WA also resulted in suppression of (i) transcriptional activity of STAT3 with or without IL-6 stimulation in both cells; (ii) dimerization of STAT3 (MDA-MB-231) and (iii) nuclear translocation of Tyr705-phosphorylated STAT3 in both cells. To our surprise, the IL-6-stimulation, either before or after WA treatment, did not have an appreciable effect on WA-mediated apoptosis in MDA-MB-231 or MCF-7 cell line. The IL-6-stimulated activation of STAT3 conferred a modest protection against WA-mediated suppression of MDA-MB-231 cell invasion. General implication of these findings is that WA can trigger apoptosis and largely inhibit cell migration/invasion of breast cancer cells even after IL-6-induced activation of STAT3, which should be viewed as a therapeutic advantage for this agent.

  J Lee , H. J Lee and C. Lee
 

As the integration scale of a chip increases, on-chip interconnects suffer from the increased area occupied by a large number of bus signals. To reduce the overhead for communication, this paper formulates a new concept of an on-chip communication approach, called phase-based interconnection, with an example protocol, system-on-chip network protocol (SNP). In the phase-based communication, a small number of signals called phase signals are used to distinguish the types of signals transmitted through the main communication channel. To identify transactions transmitted through the channel, the SNP protocol defines the allowed sequence of phases for each transaction. A theoretical framework provides conditions for a phase-based protocol to allow immediate decoding of transactions. Simulation results show that the bandwidth of SNP is greater than that of a de facto standard bus protocol although SNP has wires only about three-fifths of the standard bus protocol. Although the signal-toggling rate is increased because of the multiplexed transmission of various signals through a single communication channel, simulation results show that the increase is not significant for multimedia applications that frequently transmit burst transfers. The phase omission of SNP helps to reduce the transaction failure rate to 65% while the hardware implementation cost for the support of phase omission is negligible.

  N. E Sounni , K Dehne , L van Kempen , M Egeblad , N. I Affara , I Cuevas , J Wiesen , S Junankar , L Korets , J Lee , J Shen , C. J Morrison , C. M Overall , S. M Krane , Z Werb , N Boudreau and L. M. Coussens
  Nor E. Sounni, Kerstin Dehne, Leon van Kempen, Mikala Egeblad, Nesrine I. Affara, Ileana Cuevas, Jane Wiesen, Simon Junankar, Lidiya Korets, Jake Lee, Jennifer Shen, Charlotte J. Morrison, Christopher M. Overall, Stephen M. Krane, Zena Werb, Nancy Boudreau, and Lisa M. Coussens

Innate regulatory networks within organs maintain tissue homeostasis and facilitate rapid responses to damage. We identified a novel pathway regulating vessel stability in tissues that involves matrix metalloproteinase 14 (MMP14) and transforming growth factor beta 1 (TGFβ1). Whereas plasma proteins rapidly extravasate out of vasculature in wild-type mice following acute damage, short-term treatment of mice in vivo with a broad-spectrum metalloproteinase inhibitor, neutralizing antibodies to TGFβ1, or an activin-like kinase 5 (ALK5) inhibitor significantly enhanced vessel leakage. By contrast, in a mouse model of age-related dermal fibrosis, where MMP14 activity and TGFβ bioavailability are chronically elevated, or in mice that ectopically express TGFβ in the epidermis, cutaneous vessels are resistant to acute leakage. Characteristic responses to tissue damage are reinstated if the fibrotic mice are pretreated with metalloproteinase inhibitors or TGFβ signaling antagonists. Neoplastic tissues, however, are in a constant state of tissue damage and exhibit altered hemodynamics owing to hyperleaky angiogenic vasculature. In two distinct transgenic mouse tumor models, inhibition of ALK5 further enhanced vascular leakage into the interstitium and facilitated increased delivery of high molecular weight compounds into premalignant tissue and tumors. Taken together, these data define a central pathway involving MMP14 and TGFβ that mediates vessel stability and vascular response to tissue injury. Antagonists of this pathway could be therapeutically exploited to improve the delivery of therapeutics or molecular contrast agents into tissues where chronic damage or neoplastic disease limits their efficient delivery.

  K. D Pruitt , J Harrow , R. A Harte , C Wallin , M Diekhans , D. R Maglott , S Searle , C. M Farrell , J. E Loveland , B. J Ruef , E Hart , M. M Suner , M. J Landrum , B Aken , S Ayling , R Baertsch , J Fernandez Banet , J. L Cherry , V Curwen , M DiCuccio , M Kellis , J Lee , M. F Lin , M Schuster , A Shkeda , C Amid , G Brown , O Dukhanina , A Frankish , J Hart , B. L Maidak , J Mudge , M. R Murphy , T Murphy , J Rajan , B Rajput , L. D Riddick , C Snow , C Steward , D Webb , J. A Weber , L Wilming , W Wu , E Birney , D Haussler , T Hubbard , J Ostell , R Durbin and D. Lipman
 

Effective use of the human and mouse genomes requires reliable identification of genes and their products. Although multiple public resources provide annotation, different methods are used that can result in similar but not identical representation of genes, transcripts, and proteins. The collaborative consensus coding sequence (CCDS) project tracks identical protein annotations on the reference mouse and human genomes with a stable identifier (CCDS ID), and ensures that they are consistently represented on the NCBI, Ensembl, and UCSC Genome Browsers. Importantly, the project coordinates on manually reviewing inconsistent protein annotations between sites, as well as annotations for which new evidence suggests a revision is needed, to progressively converge on a complete protein-coding set for the human and mouse reference genomes, while maintaining a high standard of reliability and biological accuracy. To date, the project has identified 20,159 human and 17,707 mouse consensus coding regions from 17,052 human and 16,893 mouse genes. Three evaluation methods indicate that the entries in the CCDS set are highly likely to represent real proteins, more so than annotations from contributing groups not included in CCDS. The CCDS database thus centralizes the function of identifying well-supported, identically-annotated, protein-coding regions.

  S. T Kim , J. Y Park , J Lee , J. O Park , Y. S Park , H. Y Lim , W. K Kang and S. H. Park
  Objective

Malignant peritoneal mesothelioma is a rare neoplasm that accounts for ~1 per 1 million has limited data regarding its frontline therapy. We investigated the treatment outcomes in patients with malignant peritoneal mesothelioma receiving frontline cisplatin-based combination chemotherapy.

Methods

We analyzed 14 patients with malignant peritoneal mesothelioma who had been treated by frontline cisplatin-based combination chemotherapy between January 2005 and March 2009. The chemotherapeutic agent added to platinum was gemcitabine in one patient, cyclophosphamide–doxorubicin in three patients and pemetrexed in 10 patients.

Results

The confirmed overall response rate was 35.7% and the disease control rate was 71.4%. In all patients, two complete responses and three partial responses were observed (overall response rate, 35.7%). Stable disease was observed in five patients (35.7%). The median progression free survival was 4.4 months (95% CI, 0.6–9.0) and the median overall survival was 20.1 months (95% CI, 12.7–28.5). There was significant differences for progression free survival (P = 0.031) according to the different chemotherapeutic agents (pemetrexed versus non-pemetrexed agents) added to platinum. Grade 3 or 4 hematologic toxicities included leukopenia in one patient and anemia in three patients. There were no Grade 3 or 4 non-hematologic toxicities or treatment-related deaths.

Conclusion

The platinum-based combination chemotherapy showed moderate activity and a favorable toxicity profile as a frontline treatment for patients with malignant peritoneal mesothelioma. Pemetrexed in combination with platinum showed improved survival outcomes as compared with other combination regimens combined with platinum.

  H. Y Ahn , J Lee and H. J. Shin
 

After births, premature infants need a high level of medical treatments for their survivals in the neonatal intensive care unit (NICU). This separation deprives mothers of the chance to initiate an attachment process. Kangaroo care (KC) can be one of the ways to reunite mothers and their infants in the NICU and improve health outcomes. This study was conducted to investigate the effects of KC on both premature infants and their mothers. Ten sessions of 60-min KC for 3 weeks were practiced at a level III NICU at E university hospital. Infants’ body weight, height and head circumference (HC), maternal attachment and depression were measured. As a result, premature infants in KC showed higher in their height and bigger in their HC than infants in control. Maternal attachment scores were higher among the KC mothers. The results supported the beneficial effects of KC on Korean premature infants and their mothers.

  S. K Banu , J Lee , V. O Speights , A Starzinski Powitz and J. A. Arosh
 

Endometriosis is a benign chronic gynecological disease of reproductive-age women characterized by the presence of functional endometrial tissues outside the uterine cavity. It is an estrogen-dependent disease. Current treatment modalities to inhibit biosynthesis and actions of estrogen compromise menstruation, pregnancy, and the reproductive health of women and fail to prevent reoccurrence of disease. There is a critical need to identify new specific signaling modules for non-estrogen-targeted therapies for endometriosis. In our previous study, we reported that selective inhibition of cyclooxygenase-2 prevented survival, migration, and invasion of human endometriotic epithelial and stromal cells, which was due to decreased prostaglandin E2 (PGE2) production. In this study, we determined mechanisms through which PGE2 promoted survival of human endometriotic cells. Results of the present study indicate that 1) PGE2 promotes survival of human endometriotic cells through EP2 and EP4 receptors by activating ERK1/2, AKT, nuclear factor-B, and β-catenin signaling pathways; 2) selective inhibition of EP2 and EP4 suppresses these cell survival pathways and augments interactions between proapoptotic proteins (Bax and Bad) and antiapoptotic proteins (Bcl-2/Bcl-XL), facilitates the release of cytochrome c, and thus activates caspase-3/poly (ADP-ribose) polymerase-mediated intrinsic apoptotic pathways; and 3) these PGE2 signaling components are more abundantly expressed in ectopic endometriosis tissues compared with eutopic endometrial tissues during the menstrual cycle in women. These novel findings may provide an important molecular framework for further evaluation of selective inhibition of EP2 and EP4 as potential therapy, including nonestrogen target, to expand the spectrum of currently available treatment options for endometriosis in women.

  D. H Kim , J Lee , B Lee and J. W. Lee
 

Activating signal cointegrator-2 (ASC-2), a coactivator of multiple nuclear receptors and transcription factors, belongs to a steady-state complex named ASCOM (for ASC-2 complex), which contains histone H3 lysine 4 (H3K4) methyltransferase MLL3 or its paralog MLL4. ASC-2 binds to many nuclear receptors in a ligand-dependent manner through its two LxxLL motifs. Here we show that the first LxxLL motif of ASC-2 shows relatively weak but specific interaction with the nuclear receptor farnesoid X receptor (FXR) and that ASCOM plays crucial roles in FXR transactivation. Our results reveal that ASC-2, MLL3, and MLL4 are recruited to FXR target genes in a ligand-dependent manner. We further show that the recruitment of MLL3 requires ASC-2 and that FXR ligand induces not only expression of FXR-target genes but also their H3K4 trimethylation in a manner dependent on the presence of ASC-2, MLL3, and MLL4. In addition, MLL3 and MLL4 function redundantly with FXR transactivation. Correspondingly, expression of FXR target genes is partially impaired in mice expressing an enzymatically inactivated mutant form of MLL3, and these mice show disrupted bile acid homeostasis. Overall, these results suggest that ASCOM-MLL3 and ASCOM-MLL4 play redundant but essential roles in FXR transactivation via their H3K4 trimethylation activity.

  S. K Banu , J Lee , S. D Stephen , T. K Nithy and J. A. Arosh
 

In ruminants, pulsatile release of prostaglandin F2 (PGF2) from the endometrium is transported to the ovary and induces luteolysis thereby allowing new estrous cycle. Interferon tau (IFNT), a type 1 IFN secreted by the trophoblast cells of the developing conceptus, acts on endometrial luminal epithelial (LE) cells and inhibits pulsatile release of PGF2 and establishes pregnancy. One of the unknown mechanisms is that endometrial pulsatile release of PGF2 is inhibited whereas basal release of PGF2 is increased in pregnant compared with nonpregnant sheep. We have recently found that pulsatile release of PGF2 from the endometrium is regulated by prostaglandin transporter (PGT)-mediated mechanisms. We hypothesize that modulation in the endometrial pulsatile vs. basal release of PGF2 likely requires PGT-mediated selective transport, and IFNT interacts with PGT protein and modulates pulsatile vs. basal release of PGF2. The new findings of the present study are: 1) IFNT activates novel JAK-SRC kinase-EGFR-RAS-RAF-ERK1/2-early growth response (EGR)-1 signaling module in LE cells; 2) IFNT increases interactions between PGT and ERK1/2 or EGR-1 proteins and alters phosphorylation of PGT protein; 3) IFNT precludes action of protein kinase C and Ca2+ on PGT function; and 4) IFNT inhibits 80% PGT-mediated but not 20% simple diffusion-mediated release of PGF2 from the endometrial LE cells through this novel signaling module. The results of the present study provide important new insights on IFNT signaling and molecular control of PGT-mediated release of PGF2 and unravel the underlying mechanisms responsible for the increased basal release of PGF2 at the time of establishment of pregnancy in ruminants.

  M. E Rumpho , S Pochareddy , J. M Worful , E. J Summer , D Bhattacharya , K. N Pelletreau , M. S Tyler , J Lee , J. R Manhart and K. M. Soule
 

Phosphoribulokinase (PRK), a nuclear-encoded plastid-localized enzyme unique to the photosynthetic carbon reduction (Calvin) cycle, was cloned and characterized from the stramenopile alga Vaucheria litorea. This alga is the source of plastids for the mollusc (sea slug) Elysia chlorotica which enable the animal to survive for months solely by photoautotrophic CO2 fixation. The 1633-bp V. litorea prk gene was cloned and the coding region, found to be interrupted by four introns, encodes a 405-amino acid protein. This protein contains the typical bipartite target sequence expected of nuclear-encoded proteins that are directed to complex (i.e. four membrane-bound) algal plastids. De novo synthesis of PRK and enzyme activity were detected in E. chlorotica in spite of having been starved of V. litorea for several months. Unlike the algal enzyme, PRK in the sea slug did not exhibit redox regulation. Two copies of partial PRK-encoding genes were isolated from both sea slug and aposymbiotic sea slug egg DNA using PCR. Each copy contains the nucleotide region spanning exon 1 and part of exon 2 of V. litorea prk, including the bipartite targeting peptide. However, the larger prk fragment also includes intron 1. The exon and intron sequences of prk in E. chlorotica and V. litorea are nearly identical. These data suggest that PRK is differentially regulated in V. litorea and E. chlorotica and at least a portion of the V. litorea nuclear PRK gene is present in sea slugs that have been starved for several months.

  T Mihata , J Gates , M. H McGarry , J Lee , M Kinoshita and T. Q. Lee
  Background

Throwing athletes with shoulder pain have been shown to have decreased rotator cuff muscle strength. Shoulder internal impingement and labral peel-back mechanism, as may occur during the late cocking phase of throwing motion, are thought to cause rotator cuff injury and type II superior labrum anterior and posterior lesions. Therefore, the objective of this study was to assess the effect of rotator cuff muscle force on internal impingement and the peel-back of the superior labrum by quantifying maximum external rotation, glenohumeral contact pressure, and position of the cuff insertion relative to the glenoid.

Hypothesis

A change in rotator cuff muscle force will lead to increased external rotation, glenohumeral contact pressure, and overlap of the cuff insertion relative to the glenoid.

Study Design

Controlled laboratory study.

Methods

Eight fresh-frozen cadaveric shoulders were tested at the simulated late cocking position. Glenohumeral contact pressure, location of the cuff insertion relative to the glenoid, and maximum humeral external rotation angle were measured. The forces of the supraspinatus, subscapularis, and infraspinatus muscles were determined based on published clinical electromyographic data. To assess the effect of cuff muscle imbalance, each muscle force was varied. Horizontal abduction positions of 20°, 30°, and 40° with respect to the scapular plane were tested.

Results

Decreased subscapularis strength resulted in a significant increase in maximum external rotation (P <.001) and increased glenohumeral contact pressure (P <.01). The cuff insertion overlapped the edge of the glenoid at 30° and 40° of horizontal abduction for all muscle loading conditions.

Conclusion

Decreased subscapularis muscle strength in the position simulating the late cocking phase of throwing motion results in increased maximum external rotation and also increased glenohumeral contact pressure.

Clinical Relevance

Athletes with decreased subscapularis muscle strength, such as fatigue with repetitive throwing, may be more susceptible to rotator cuff tears and type II superior labrum anterior and posterior lesions. Subscapularis muscle strengthening exercises may be beneficial for preventing these injuries.

 
 
 
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