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Items 1 to 10 of about 28170
1. Oh IK, Kim S, Oh J, Huh K: Long-term visual outcome of arteriovenous adventitial sheathotomy on branch retinal vein occlusion induced macular edema. Korean J Ophthalmol; 2008 Mar;22(1):1-5
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  • [Title] Long-term visual outcome of arteriovenous adventitial sheathotomy on branch retinal vein occlusion induced macular edema.
  • PURPOSE: To evaluate long-term visual outcome of arteriovenous adventitial sheathotomy in BRVO-induced macular edema.
  • METHODS: The visual outcomes of 8 patients following vitrectomy with arteriovenous adventitial sheathotomy for BVO-induced macular edema (surgery group) were retrospectively evaluated.
  • The three-year post-operative visual acuity of the surgery group was compared with that of the conservatively managed controls.
  • RESULTS: All patients were followed for a minimum of 36 months.
  • Mean BCVA (logMAR) in the surgery group changed from 1.10+/-0.34 to 1.19+/-0.70 and to 0.80+/-0.36 at 12 and 36 months, respectively (p=0.959 at 12 months, p=0.018 at 36 months).
  • In the control group, visual acuity improved from 1.15+/-0.43 to 0.43+/-0.44 and to 0.43+/-0.39 at 12 and 36 months, respectively (p=0.015 at 12 months, at p=0.003 at 36 months).
  • A strong trend toward better visual acuity at 12 months and final examination was observed for controls. (surgery vs. control group, p=0.052 at 12 months, p=0.066 at 36 months).
  • CONCLUSIONS: Considering the favorable natural course of BVO and the unproven effect of reperfusion on macular edema, surgical efficacy of arteriovenous adventitial sheathotomy requires further evaluation.
  • [MeSH-major] Connective Tissue / surgery. Macular Edema / surgery. Retinal Vein Occlusion / surgery. Visual Acuity / physiology. Vitrectomy / methods
  • [MeSH-minor] Aged. Decompression, Surgical / methods. Female. Humans. Male. Middle Aged. Retinal Artery. Retinal Vein. Retrospective Studies. Treatment Outcome

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  • [Cites] Br J Ophthalmol. 2003 Nov;87(11):1329-32 [14609825.001]
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  • [Cites] Arch Ophthalmol. 1988 Oct;106(10):1469-71 [3178558.001]
  • [Cites] Retina. 1999;19(1):1-5 [10048366.001]
  • [Cites] Am J Ophthalmol. 2004 Dec;138(6):907-14 [15629280.001]
  • [Cites] Am J Ophthalmol. 2006 May;141(5):876-883 [16527226.001]
  • [Cites] Am J Ophthalmol. 1984 Sep 15;98(3):271-82 [6383055.001]
  • (PMID = 18323698.001).
  • [ISSN] 1011-8942
  • [Journal-full-title] Korean journal of ophthalmology : KJO
  • [ISO-abbreviation] Korean J Ophthalmol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Korea (South)
  • [Other-IDs] NLM/ PMC2629947
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2. Oh J, Kim GD, Kim S, Lee SK: Antofine, a natural phenanthroindolizidine alkaloid, suppresses angiogenesis via regulation of AKT/mTOR and AMPK pathway in endothelial cells and endothelial progenitor cells derived from mouse embryonic stem cells. Food Chem Toxicol; 2017 Sep;107(Pt A):201-207
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  • [Title] Antofine, a natural phenanthroindolizidine alkaloid, suppresses angiogenesis via regulation of AKT/mTOR and AMPK pathway in endothelial cells and endothelial progenitor cells derived from mouse embryonic stem cells.
  • Although antofine, a natural phenanthroindolizidine alkaloid, exerts potential biological activities, including anticancer effect and anti-angiogenic activity, the underlying mechanisms have not yet been investigated.
  • In the present study, the inhibitory effect of antofine on angiogenesis was determined in cultured mouse embryonic stem (mES)/embryoid body (EB)-derived endothelial cells and vascular endothelial growth factor (VEGF)-induced human umbilical vein endothelial cells (HUVECs).
  • Antofine effectively inhibited VEGF-induced cell migration and tube formation of HUVECs.
  • Antofine also significantly decreased ex vivo microvessel sprouting in cultured mouse aortic rings, and inhibited the vascular formation and platelet/endothelial cell adhesion molecule (PECAM) expression of mES/EB-derived cells in 3-D collagen gel.
  • The underlying mechanism of anti-angiogenic activity of antofine was, in part, associated with the modulation of AKT/mTOR and AMP-activated protein kinase (AMPK) signaling in VEGF-stimulated HUVECs.
  • [MeSH-major] AMP-Activated Protein Kinases / metabolism. Angiogenesis Inhibitors / pharmacology. Endothelial Progenitor Cells / drug effects. Indoles / pharmacology. Mouse Embryonic Stem Cells / drug effects. Neovascularization, Pathologic / metabolism. Phenanthrolines / pharmacology. Proto-Oncogene Proteins c-akt / metabolism. TOR Serine-Threonine Kinases / metabolism
  • [MeSH-minor] Animals. Cell Proliferation / drug effects. Humans. Indolizines / pharmacology. Mice. Signal Transduction / drug effects. Vascular Endothelial Growth Factor A / genetics. Vascular Endothelial Growth Factor A / metabolism

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  • [Copyright] Copyright © 2017 The Author(s). Published by Elsevier Ltd.. All rights reserved.
  • (PMID = 28666888.001).
  • [ISSN] 1873-6351
  • [Journal-full-title] Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association
  • [ISO-abbreviation] Food Chem. Toxicol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Indoles; 0 / Indolizines; 0 / Phenanthrolines; 0 / Vascular Endothelial Growth Factor A; 0 / antofine; 0 / phenanthroindolizidine; EC 2.7.1.1 / TOR Serine-Threonine Kinases; EC 2.7.11.1 / AMP-Activated Protein Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt
  • [Keywords] NOTNLM ; AKT/mTOR / AMPK / Angiogenesis / Antofine / HUVECs
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3. Ko YG, Kang YS, Park H, Seol W, Kim J, Kim T, Park HS, Choi EJ, Kim S: Apoptosis signal-regulating kinase 1 controls the proapoptotic function of death-associated protein (Daxx) in the cytoplasm. J Biol Chem; 2001 Oct 19;276(42):39103-6
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  • [Title] Apoptosis signal-regulating kinase 1 controls the proapoptotic function of death-associated protein (Daxx) in the cytoplasm.
  • Although Daxx (death-associated protein) was first reported to mediate the apoptotic signal from Fas to JNK in the cytoplasm, other data suggested that Daxx is mainly located in the nucleus as a transcriptional regulator.
  • Here, we demonstrated that cellular localization of Daxx could be determined by the relative concentration of a proapoptotic kinase, apoptosis signal-regulating kinase 1 (ASK1) by using immunofluorescence and transcriptional reporter assay.
  • ASK1 sequestered Daxx in the cytoplasm and inhibited the repressive activity of Daxx in transcription.
  • In addition, Daxx was bound to the activated Fas only in the presence of ASK1, accelerating the Fas-mediated apoptosis.
  • These results suggest that Daxx requires ASK1 for its cytoplasmic localization and Fas-mediated signaling.
  • Taken together, we could conclude that ASK1 controls the dual function of Daxx as a transcriptional repressor in the nucleus and as a proapoptotic signal mediator in the cytoplasm.
  • [MeSH-major] Apoptosis. Arabidopsis Proteins. Carrier Proteins / biosynthesis. Cytoplasm / metabolism. Intracellular Signaling Peptides and Proteins. MAP Kinase Kinase Kinases / metabolism. Nuclear Proteins. Plant Proteins / metabolism
  • [MeSH-minor] Adaptor Proteins, Signal Transducing. Cell Line. DNA / metabolism. Genes, Dominant. Genes, Reporter. Humans. MAP Kinase Kinase Kinase 5. Microscopy, Fluorescence. Plasmids / metabolism. Precipitin Tests. Protein Binding. Signal Transduction. Transcription, Genetic. Transfection

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  • (PMID = 11495919.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ASK1 protein, Arabidopsis; 0 / Adaptor Proteins, Signal Transducing; 0 / Arabidopsis Proteins; 0 / Carrier Proteins; 0 / DAXX protein, human; 0 / Intracellular Signaling Peptides and Proteins; 0 / Nuclear Proteins; 0 / Plant Proteins; 9007-49-2 / DNA; EC 2.7.11.25 / MAP Kinase Kinase Kinase 5; EC 2.7.11.25 / MAP Kinase Kinase Kinases; EC 2.7.11.25 / MAP3K5 protein, human
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4. Kang J, Kim T, Ko YG, Rho SB, Park SG, Kim MJ, Kwon HJ, Kim S: Heat shock protein 90 mediates protein-protein interactions between human aminoacyl-tRNA synthetases. J Biol Chem; 2000 Oct 13;275(41):31682-8
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  • [Title] Heat shock protein 90 mediates protein-protein interactions between human aminoacyl-tRNA synthetases.
  • Heat shock protein 90 (hsp90) is a molecular chaperone responsible for protein folding and maturation in vivo.
  • Interaction of hsp90 with human glutamyl-prolyl-tRNA synthetase (EPRS) was found by genetic screening, co-immunoprecipitation, and in vitro binding experiments.
  • This interaction was sensitive to the hsp90 inhibitor, geldanamycin, and also ATP, suggesting that the chaperone activity of hsp90 is required for interaction with EPRS.
  • Interaction of EPRS with hsp90 was targeted to the region of three tandem repeats linking the two catalytic domains of EPRS that is also responsible for the interaction with isoleucyl-tRNA synthetase (IRS).
  • Interaction of EPRS and IRS also depended on the activity of hsp90, implying that their association was mediated by hsp90.
  • EPRS and IRS form a macromolecular protein complex with at least six other tRNA synthetases and three cofactors. hsp90 preferentially binds to most of the complex-forming enzymes rather than those that are not found in the complex.
  • In addition, inactivation of hsp90 interfered with the in vivo incorporation of the nascent aminoacyl-tRNA synthetases into the multi-ARS complex.
  • Thus, hsp90 appears to mediate protein-protein interactions of mammalian tRNA synthetases.
  • [MeSH-major] Amino Acyl-tRNA Synthetases / metabolism. HSP90 Heat-Shock Proteins / metabolism
  • [MeSH-minor] Adenosine Triphosphate / metabolism. Adenosine Triphosphate / pharmacology. Animals. Benzoquinones. Binding Sites. Cattle. HeLa Cells. Humans. Hydroxamic Acids / pharmacology. Lactams, Macrocyclic. Lactones / pharmacology. Macrolides. Macromolecular Substances. Precipitin Tests. Protein Binding / drug effects. Quinones / pharmacology. Substrate Specificity. Tandem Repeat Sequences. Two-Hybrid System Techniques. Yeasts

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  • (PMID = 10913161.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Benzoquinones; 0 / HSP90 Heat-Shock Proteins; 0 / Hydroxamic Acids; 0 / Lactams, Macrocyclic; 0 / Lactones; 0 / Macrolides; 0 / Macromolecular Substances; 0 / Quinones; 12772-57-5 / monorden; 3X2S926L3Z / trichostatin A; 8L70Q75FXE / Adenosine Triphosphate; EC 6.1.1.- / Amino Acyl-tRNA Synthetases; EC 6.1.1.- / glutamyl-prolyl-tRNA synthetase; Z3K3VJ16KU / geldanamycin
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5. Oh S, Lewis B, Watson A, Kim S, Kim T: The effect of beam interruption during FFF-VMAT plans for SBRT. Australas Phys Eng Sci Med; 2017 Oct 02;
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  • [Title] The effect of beam interruption during FFF-VMAT plans for SBRT.
  • To investigate the dosimetric effect of intended beam interruption during volumetric modulated arc therapy (VMAT) with flattening filter free (FFF) beam for exploring the possibility of deep inspiration breath hold stereotactic body radiation therapy (SBRT).
  • A total of ten SBRT plans with 6 and 10 MV FFF beams were retrospectively selected.
  • All plans consisted of four partial arcs, except one plan with six partial arcs.
  • We delivered the plans using a Varian Truebeam™ with three different scenarios; without interruption (0int), with one intentional interruption (1int), or with two intentional interruptions (2int), per each partial arc.
  • The treatment log files were exported from the treatment console, and the variations in delivered MU were evaluated at the beam interruption angles.
  • The dose distributions were also measured using a 3D cylindrical diode array detector, ArcCHECK™.
  • The 2D global gamma evaluations were performed, compared to the planned dose distribution, with 3%/3 and 4%/2 mm passing criterion.
  • The dose difference (DD) was also determined between uninterrupted and interrupted data with 3, 2, 1, and 0.5% of global maximum dose.
  • The interruption caused a total increase of 0.14 ± 0.05% and 0.25 ± 0.08% of the total planned MU, ranging from 1746 to 3261 MU, at the interrupted angles in 1int and 2int, respectively.
  • All global gamma passing rates satisfied our clinical threshold of 90%, and the differences of passing rates were less than 0.3% on average with both criterions.
  • All measured 1int and 2int data were within 3% DD from 0int measured data.
  • For 6 MV FFF beams, the average passing rate with 2, 1, and 0.5% DD were 99.9 ± 0.2%, 92.3 ± 12.0%, and 81.9 ± 24.9%, respectively, between 0int and 1int, and 99.8 ± 0.4%, 92.1%12.4%, and 80.7 ± 26.5%, respectively, between 0int and 2int.
  • For 10 MV FFF beams, the average passing rate with 2, 1, and 0.5% DD were 100.0 ± 0.2%, 95.4 ± 9.4% and 87.0 ± 19.8%, respectively, between 0int and 1int, and 99.9 ± 0.3%, 95.4 ± 9.7%, and 87.2 ± 21.3% between 0int and 2int.
  • The dosimetric impact of beam interruption was investigated with small field and high dose rate FFF-VMAT SBRT plans.
  • The delivered dose distributions with up to 12 interruptions per plan were still clinically acceptable.
  • Only minimal changes were observed in Gamma, DD, and log file analysis.

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  • (PMID = 28971344.001).
  • [ISSN] 1879-5447
  • [Journal-full-title] Australasian physical & engineering sciences in medicine
  • [ISO-abbreviation] Australas Phys Eng Sci Med
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Keywords] NOTNLM ; Beam interruption / Cylindrical diode array detector / DIBH / Deep inspiration breath hold / FFF / SBRT / VMAT
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6. Kim TI, Kim SW, Kim S, Kim T, Kim EK: Inhibition of experimental corneal neovascularization by using subconjunctival injection of bevacizumab (Avastin). Cornea; 2008 Apr;27(3):349-52
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  • [Title] Inhibition of experimental corneal neovascularization by using subconjunctival injection of bevacizumab (Avastin).
  • PURPOSE: To evaluate the effect of subconjunctival bevacizumab (Avastin) administration on corneal neovascularization (NV) in rabbits.
  • METHODS: NV was induced by placing a suture at the corneal periphery of the right eye of 20 rabbits.
  • Immediately after suturing and again 1 week later, rabbits were divided into 2 groups and administered a subconjunctival injection of normal saline (control) or bevacizumab (Avastin; 5 mg/0.2 mL), respectively.
  • On day 14, digital photographs of the cornea were taken and analyzed to determine the area of the cornea covered by NV.
  • In addition, immunohistochemical analysis was used to determine CD31 and vascular endothelial growth factor (VEGF) expression in corneal tissue.
  • RESULTS: Analysis of digital photographs showed that there was less corneal NV in bevacizumab-treated eyes than in controls (P < 0.001, Mann-Whitney U test).
  • In addition, there was less staining for VEGF and CD31 in corneas from bevacizumab-treated eyes than in control eyes.
  • Subconjunctival bevacizumab injections were not associated with any complications during observation.
  • CONCLUSIONS: Subconjunctival bevacizumab administration decreased suture-induced corneal neovascularization in rabbits.
  • [MeSH-major] Angiogenesis Inhibitors / administration & dosage. Antibodies, Monoclonal / administration & dosage. Corneal Neovascularization / drug therapy. Disease Models, Animal
  • [MeSH-minor] Animals. Antibodies, Monoclonal, Humanized. Antigens, CD31 / metabolism. Bevacizumab. Conjunctiva. Fluorescent Antibody Technique, Indirect. Injections. Rabbits. Vascular Endothelial Growth Factor A / metabolism

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  • (PMID = 18362666.001).
  • [ISSN] 0277-3740
  • [Journal-full-title] Cornea
  • [ISO-abbreviation] Cornea
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antigens, CD31; 0 / Vascular Endothelial Growth Factor A; 2S9ZZM9Q9V / Bevacizumab
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7. Ding C, Yu H, Yu H, Qin H: TP53 codon 72 polymorphism with hepatocellular carcinoma: a metaanalysis. J Int Med Res; 2012;40(2):446-54
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  • [Title] TP53 codon 72 polymorphism with hepatocellular carcinoma: a metaanalysis.
  • OBJECTIVE: The association between codon 72 polymorphism of the tumour protein p53 (TP53) gene - which results in a missense mutation of arginine (R) to proline (P) - and susceptibility to hepatocellular carcinoma (HCC) is controversial.
  • A metaanalysis was performed in order to define this relationship more precisely.
  • METHODS: Published studies of TP53 codon 72 polymorphism and the risk of HCC were identified.
  • Data were extracted, and summary odds ratios (OR) and 95% confidence intervals (95% CI) were calculated.
  • Pooled ORs were determined for an additive model (R/R versus P/P), a dominant model ([R/R + R/P] versus P/P) and a recessive model (R/R versus [R/P + P/P]).
  • RESULTS: The meta-analysis included seven case-control studies (total 1511 cases and 2165 controls).
  • The risk of cancer was significantly decreased in the overall dominant model and the dominant model in Asian populations.
  • A significantly decreased risk was found for all models in hospital-based but not population-based studies.
  • There was no association between polymorphism and cancer risk when data were stratified according to hepatitis B or C virus infection status.
  • CONCLUSION: The TP53 codon 72 polymorphism may be a risk factor for HCC.
  • [MeSH-major] Carcinoma, Hepatocellular / genetics. Genes, p53. Hepatitis B / complications. Hepatitis C / complications. Liver Neoplasms / genetics. Tumor Suppressor Protein p53 / genetics
  • [MeSH-minor] Aflatoxin B1 / toxicity. Alcohol Drinking / adverse effects. Asian Continental Ancestry Group / genetics. Case-Control Studies. Female. Gene Frequency. Genetic Predisposition to Disease. Genotype. Humans. Male. Polymorphism, Single Nucleotide. Risk. Risk Factors

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  • [CommentIn] J Int Med Res. 2013 Apr;41(2):519-20 [23569040.001]
  • (PMID = 22613405.001).
  • [ISSN] 1473-2300
  • [Journal-full-title] The Journal of international medical research
  • [ISO-abbreviation] J. Int. Med. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Meta-Analysis; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / TP53 protein, human; 0 / Tumor Suppressor Protein p53; 9N2N2Y55MH / Aflatoxin B1
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8. Kim SJ, Oh J, Kang KA, Kim S: Development and evaluation of simulation-based fever management module for children with febrile convulsion. Nurse Educ Today; 2014 Jun;34(6):1005-11
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  • [Title] Development and evaluation of simulation-based fever management module for children with febrile convulsion.
  • BACKGROUND: A reliable and valid checklist for the evaluation of simulation learning outcomes has great value in nursing education.
  • This study focuses on simulation-based fever management module including checklist for febrile convulsion in pediatric nursing.
  • PURPOSES: This study has two aims;.
  • (a) to develop a simulation-based fever management module for treating children with febrile convulsion, and (b) to evaluate students' performance and satisfaction.
  • PARTICIPANTS: A convenient sample of 147 senior nursing students from two nursing schools in South Korea participated in this study from April 29 to June 14, 2013.
  • METHODS: This study was a three-stage process: developing the simulation-based module including algorithm with scenarios, items in checklist, and contents of debriefing (Stage I), performing simulation and debriefing for nursing students (Stage II), and evaluating the evaluation checklist of simulation performance and satisfaction of nursing students (Stage III).
  • Student satisfaction was measured using the Satisfaction of Simulations Experience [SSE] scale.
  • Debriefing data were analyzed using the Matrix Method.
  • RESULTS: A scenario script was created to treat the patient's health issues.
  • The algorithm proceeded as follows: identification of patient's condition (Step I), nursing interventions (Step II), and outcome evaluation and feedback (Step III).
  • The total mean score of the evaluation checklist was 2.67 (±.32).
  • The debriefing categories were as follows: non-technical skills, self-efficacy, critical thinking, and technical skills.
  • The total mean score of the SSE was 4.48 (±.42).
  • CONCLUSION: This study provides a blueprint for simulation-based practice for both nursing educators and nursing students.
  • Further studies of checklists used in different contexts would be valuable for expanding upon this research.
  • [MeSH-major] Disease Management. Education, Nursing, Baccalaureate. Seizures, Febrile / nursing. Simulation Training
  • [MeSH-minor] Algorithms. Educational Measurement. Humans. Infant. Manikins. Pediatric Nursing. Republic of Korea

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  • [Copyright] Copyright © 2013 Elsevier Ltd. All rights reserved.
  • (PMID = 24321166.001).
  • [ISSN] 1532-2793
  • [Journal-full-title] Nurse education today
  • [ISO-abbreviation] Nurse Educ Today
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article
  • [Publication-country] Scotland
  • [Keywords] NOTNLM ; Child / Febrile convulsion / Nursing education / Patient simulation
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9. Oh J, Rhee HJ, Kim S, Kim SB, You H, Kim JH, Na DS: Annexin-I inhibits PMA-induced c-fos SRE activation by suppressing cytosolic phospholipase A2 signal. FEBS Lett; 2000 Jul 21;477(3):244-8
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  • [Title] Annexin-I inhibits PMA-induced c-fos SRE activation by suppressing cytosolic phospholipase A2 signal.
  • Annexin-I (ANX-I) is a 37-kDa protein with a calcium-dependent phospholipid-binding property.
  • Previously we have observed the inhibition of cytosolic phospholipase A2 (cPLA2) by ANX-I in the studies using purified recombinant ANX-I, and proposed a specific interaction model for the mechanism of cPLA2 inhibition by ANX-I [Kim et al. (1994) FEBS Lett.
  • 343, 251-255].
  • Here we have studied the role of ANX-I in the cPLA2 signaling pathway by transient transfection assay.
  • The stimulation of Rat2 fibroblast cells with phorbol 12-myristate 13-acetate (PMA) induced the c-fos serum response element (SRE).
  • The SRE stimulation by PMA was dramatically reduced by (1) pretreatment with a cPLA2-specific inhibitor, arachidonyltrifluoromethyl ketone, or (2) co-transfection with antisense cPLA2 oligonucleotide, indicating that the SRE activation was through cPLA2 activation.
  • Co-transfection with an ANX-I expression vector also reduced the SRE stimulation by PMA, suggesting the inhibition of cPLA2 by ANX-I.
  • The active domain of ANX-I was mapped using various deletion mutants.
  • ANX-I(1-113) and ANX-I(34-346) were fully active, whereas ANX-I(114-346) abolished the activity.
  • Therefore the activity was in the amino acid 34 to 113 region, which corresponds to the conserved domain I of ANX-I.
  • [MeSH-major] Annexin A1 / pharmacology. Cytosol / drug effects. Genes, fos. Phospholipases A / antagonists & inhibitors. Signal Transduction / drug effects. Tetradecanoylphorbol Acetate / pharmacology
  • [MeSH-minor] Animals. Base Sequence. Cell Line. Oligonucleotides. Phospholipases A2. Rats

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  • (PMID = 10908728.001).
  • [ISSN] 0014-5793
  • [Journal-full-title] FEBS letters
  • [ISO-abbreviation] FEBS Lett.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] NETHERLANDS
  • [Chemical-registry-number] 0 / Annexin A1; 0 / Oligonucleotides; EC 3.1.1.- / Phospholipases A; EC 3.1.1.4 / Phospholipases A2; NI40JAQ945 / Tetradecanoylphorbol Acetate
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10. Yu H: [Qualitative research and clinical study on cancer]. Zhongguo Zhong Xi Yi Jie He Za Zhi; 2008 Feb;28(2):169-71
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Qualitative research and clinical study on cancer].
  • Tumor is one of the fateful diseases that human must confront.
  • Currently, quantitative research is still the principal body of the research on cancer.
  • Qualitative research can compensate the limitations of quantitative research in evaluating therapeutic effects on cancer, it can profoundly understand the attitude, experience, confidence, presumable problems and obstacles of doctors and patients to the therapy.
  • This article introduces the necessity and general situation of development in applying qualitative research methods in the researches on tumor, and the main problems and developing tendency for extending in China.

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  • (PMID = 18386584.001).
  • [ISSN] 1003-5370
  • [Journal-full-title] Zhongguo Zhong xi yi jie he za zhi Zhongguo Zhongxiyi jiehe zazhi = Chinese journal of integrated traditional and Western medicine
  • [ISO-abbreviation] Zhongguo Zhong Xi Yi Jie He Za Zhi
  • [Language] CHI
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
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