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Y-M Park

Publications and source records attributed to Y-M Park.

7 recordsLinked to original sources
PubMed2007

Long-term effects of a structured intensive diabetes education programme (SIDEP) in patients with Type 2 diabetes mellitus--a 4-year follow-up study.

AIMS: Patient education is a very important part of diabetes care. However, until now, little data has been presented about the long-term effectiveness of structured intensive diabetes education programmes (SIDEP) for people with Type 2 diabetes mellitus. METHODS: People with Type 2 diabetes (n = 547) hospitalized from December 1999 to December 2000 were randomly assigned to two groups. Two hundred and nineteen patients undertook an inpatient SIDEP and the remaining patients received conventional glycaemic control without intensive education. After discharge, all patients were monitored regularly. Laboratory data were obtained, and adherence to self-care behaviour was determined on a five-point scale by questionnaires completed annually. RESULTS: Of the patients who completed the SIDEP, 160 (73.1%) were followed up for more than 4 years. The mean HbA(1c) (7.9 +/- 1.2 vs. 8.7 +/- 1.6%; P < 0.05) and the frequency of hospitalization related to diabetes per patient per year (0.3 +/- 0.6 vs. 0.8 +/- 0.9; P < 0.05) was significantly lower in the SIDEP group than in the control group. The SIDEP group adhered more closely to self-care behaviour than the control group over 4 years (P < 0.05). People with Type 2 diabetes mellitus of longer duration and those treated with insulin had poorer HbA(1c) at follow-up. CONCLUSIONS: A well-designed, intensive patient education programme is necessary for people with diabetes. However, regular and sustained reinforcement with encouragement is also required to maintain optimal glycaemic control, especially in insulin-treated patients.

Adult↗
PubMed2006

Enhanced selenium effect on growth arrest by BiP/GRP78 knockdown in p53-null human prostate cancer cells.

Redox modification of thiol/disulfide interchange in proteins by selenium could lead to protein unfolding. When this occurs in the endoplasmic reticulum (ER), a process known as unfolded protein response (UPR) is orchestrated for survival through activation of PERK-eIF2alpha (PERK: double-stranded RNA-activated protein kinase-like ER kinase; eIF2alpha: eucaryotic initiation factor 2alpha), ATFalpha (ATFalpha: activating transcription factor 6) and inositol requiring 1 (IRE1)-x-box-binding protein 1 (XBP1) signalings. All three UPR transducer pathways were upregulated very rapidly when PC-3 cells were exposed to selenium. These changes were accompanied by increased expression of UPR target genes, including immunoglobulin heavy chain-binding protein/glucose-regulated protein, 78 kDa and CCAAT/enhancer binding protein-homologous protein/growth arrest- and DNA damage-inducible gene (CHOP/GADD153). Induction of BiP/GRP78, an ER-resident chaperone, is part of the damage control mechanism, while CHOP/GADD153 is a transcription factor associated with growth arrest and apoptosis in the event of prolonged ER stress. Knocking down BiP/GRP78 induction by small interference RNA produced a differential response of the three transducers to selenium, suggesting that the signaling intensity of each transducer could be fine-tuned depending on BiP/GRP78 availability. In the presence of selenium, CHOP/GADD153 expression was raised even higher by BiP/GRP78 knockdown. Under this condition, the selenium effect on wild-type p53-activated fragment p21 (p21(WAF)), cyclin-dependent kinase (CDK)1 and CDK2 was also magnified in a manner consistent with enhanced cell growth arrest. Additional experiments with CHOP/GADD153 siRNA knockdown strongly suggested that CHOP/GADD153 may play a positive role in upregulating the expression of p21(WAF) in a p53-independent manner (PC-3 cells are p53 null). Collectively, the above findings support the idea that UPR could be an important mechanism in mediating the anticancer activity of selenium.

CDC2 Protein Kinase↗
PubMed2005

Intramedullary clear cell meningioma.

Intramedullary clear cell meningioma (CCM), which is more aggressive than other meningioma variants, is extremely rare. To date, only one case of such a spinal tumour has been documented. We report the first case of an intramedullary CCM originating in the thoracic region of the spinal cord.

Aged↗
PubMed2004

Identification of T-cell epitopes of Porphyromonas gingivalis heat-shock-protein 60 in periodontitis.

The heat shock proteins (hsp) of bacterial species are considered to be involved in regulating the autoimmune mechanism in human diseases due to the considerable homology of their sequences with human hsp. To elucidate how stress proteins contribute to the immunopathogenesis of periodontitis, mononuclear cells from gingival connective tissue of 10 periodontitis patients were simulated with Porphyromonas gingivalis hsp60. T-cell lines reactive to P. gingivalis hsp60 were established from each patient to define T-cell epitope specificities. Anti-P. gingivalis IgG antibody titres were elevated in all patients. We could establish P. gingivalis hsp-reactive T-cell lines from gingival mononuclear cells that were mixtures of CD4+ and CD8+ cells. Of 108 overlapping synthetic peptides spanning the whole P. gingivalis hsp60 molecule, 10 peptides with epitope specificities for T-cells were identified, and were identical to those reported be B-cell epitopes in periodontitis.

Adult↗
PubMed2004

Epitope mapping of Porphyromonas gingivalis heat-shock protein and human heat-shock protein in human atherosclerosis.

To identify T- and/or cross-reactive B-cell epitopes of P. gingivalis and human heat-shock protein (HSP)60 in atherosclerosis patients, we synthesized 104 overlapping synthetic peptides spanning whole molecules of P. gingivalis HSP60 and human HSP60, respectively. T-cell epitopes of P. gingivalis HSP were identified with the use of previously established P. gingivalis HSP-reactive T-cell lines. B-cell epitopes of P. gingivalis HSP60 and human HSP60 were identified by the use of patients' sera. Anti-P. gingivalis, anti-P. gingivalis HSP60, or anti-human HSP60 IgG antibody titers were higher in the atherosclerosis patients compared with the healthy subjects. Five immunodominant peptides of P. gingivalis HSP60, identified as T-cell epitopes, were also found to be B-cell epitopes. Moreover, 6 cross-reactive B-cell epitopes of human HSP60 were identified. It was concluded that P. gingivalis HSP60 might be involved in the immunoregulatory process of atherosclerosis, with common T- and/or B-cell epitope specificities and with cross-reactivity with human HSP60.

Aged↗
PubMed2003

Characterization of blaCMY-10 a novel, plasmid-encoded AmpC-type beta-lactamase gene in a clinical isolate of Enterobacter aerogenes.

AIMS: We report the description of a novel plasmid-encoded AmpC beta-lactamase gene (blaCMY-10) from Enterobacter aerogenes K9911729 that was isolated from a patient suffering from pneumonia in South Korea. METHODS AND RESULTS: Using antibiotic susceptibility testing, plasmid analysis, transconjugation and Southern blot analysis, the cefoxitin resistance phenotype reflects the presence of a large plasmid [pYMG-1 (130 kb)] in Ent. aerogenes K9911729. One beta-lactamase with the pI of 8.0 from transconjugant of Ent. aerogenes K9911729 was identified by isoelectric focusing on a gel. A 1475 bp DNA fragment containing the blaCMY-10 gene, identified on pYMG-1 of Ent. aerogenes K9911729, was sequenced and an open reading frame coding for 382 amino acid, CMY-10, was found. The 37 class C beta-lactamases were subclassified into 1a to 1j and CMY-10 into 1a by phylogenetic analysis. A sequence identical to the common regions in In6, In7 and a novel integron from pSAL-1 was found upstream from blaCMY-10 gene at nucleotide 1-71. CONCLUSIONS: These results clearly show that blaCMY-10 gene belongs to the group of ampC-related bla genes. Homology analysis among AmpC enzymes or ampC genes implied that integration of the chromosomal ampC gene into a large resident plasmid, followed by transconjugation, was involved in the evolution of blaCMY-10 gene. SIGNIFICANCE AND IMPACT OF THE STUDY: The first identification of the blaCMY-10 gene is of concern as chromosomal beta-lactamases may cause serious therapeutic problems if their genes are translocated onto plasmids.

Base Sequence↗