Search tips
Search criteria

Results 1-3 (3)

Clipboard (0)

Select a Filter Below

more »
Year of Publication
Document Types
1.  Epidemiological Study on the Incidence of Herpes Zoster in Nearby Cheonan 
The Korean Journal of Pain  2015;28(3):193-197.
Herpes Zoster is a disease that occurs after the virus is reactivated due to infection of the varicella virus in childhood. Risk factors are advanced age, malignant neoplasm, organ transplantation, immunosuppressive agents taking are known. The purpose of this study was to investigate the relationship between the seasonal effect and other risk factors on the incidence of herpes zoster.
The medical records of 1,105 patients admitted to the outpatient diagnosed with herpes zoster were retrospectively examined. The patients' sex, age, dermatome, onset, underlying disease, residential areas were collected.
The incidence of women outnumbered men and increased for those above the age of 50. The number of occurrences of herpes zoster patients was higher in the spring and summer than in winter. Unlike men, women had the most frequent outbreaks in March. The most common occurrence of dermatome is in the thoracic region. The number of occurrence was similar on the left as the right.
In this study, herpes zoster occurs more often in women than in men and more frequently occurs in women in the spring and summer.
PMCID: PMC4500783  PMID: 26175879
Age; Epidemiology; Herpes zoster; Incidence; Seasons; Sex
2.  Role of NADH: quinone oxidoreductase-1 in the tight junctions of colonic epithelial cells 
BMB Reports  2014;47(9):494-499.
NADH:quinone oxidoreductase 1 (NQO1) is known to be involved in the regulation of energy synthesis and metabolism, and the functional studies of NQO1 have largely focused on metabolic disorders. Here, we show for the first time that compared to NQO1-WT mice, NQO1-KO mice exhibited a marked increase of permeability and spontaneous inflammation in the gut. In the DSS-induced colitis model, NQO1-KO mice showed more severe inflammatory responses than NQO1-WT mice. Interestingly, the transcript levels of claudin and occludin, the major tight junction molecules of gut epithelial cells, were significantly decreased in NQO1-KO mice. The colons of NQO1-KO mice also showed high levels of reactive oxygen species (ROS) and histone deacetylase (HDAC) activity, which are known to affect transcriptional regulation. Taken together, these novel findings indicate that NQO1 contributes to the barrier function of gut epithelial cells by regulating the transcription of tight junction molecules. [BMB Reports 2014;47(9): 494-499]
PMCID: PMC4206724  PMID: 24393524
Barrier dysfunction of epithelial cells; Chromosome condensation; Claudin-1; Gut epithelial cell tight junction; Gut inflammation; Histone acetylation/deacetylation; NQO1 knockout mice; Occludin; Transcription
3.  The Insect Peptide Coprisin Prevents Clostridium difficile-Mediated Acute Inflammation and Mucosal Damage through Selective Antimicrobial Activity▿ 
Antimicrobial Agents and Chemotherapy  2011;55(10):4850-4857.
Clostridium difficile-associated diarrhea and pseudomembranous colitis are typically treated with vancomycin or metronidazole, but recent increases in relapse incidence and the emergence of drug-resistant strains of C. difficile indicate the need for new antibiotics. We previously isolated coprisin, an antibacterial peptide from Copris tripartitus, a Korean dung beetle, and identified a nine-amino-acid peptide in the α-helical region of it (LLCIALRKK) that had antimicrobial activity (J.-S. Hwang et al., Int. J. Pept., 2009, doi:10.1155/2009/136284). Here, we examined whether treatment with a coprisin analogue (a disulfide dimer of the nine peptides) prevented inflammation and mucosal damage in a mouse model of acute gut inflammation established by administration of antibiotics followed by C. difficile infection. In this model, coprisin treatment significantly ameliorated body weight decreases, improved the survival rate, and decreased mucosal damage and proinflammatory cytokine production. In contrast, the coprisin analogue had no apparent antibiotic activity against commensal bacteria, including Lactobacillus and Bifidobacterium, which are known to inhibit the colonization of C. difficile. The exposure of C. difficile to the coprisin analogue caused a marked increase in nuclear propidium iodide (PI) staining, indicating membrane damage; the staining levels were similar to those seen with bacteria treated with a positive control for membrane disruption (EDTA). In contrast, coprisin analogue treatment did not trigger increases in the nuclear PI staining of Bifidobacterium thermophilum. This observation suggests that the antibiotic activity of the coprisin analogue may occur through specific membrane disruption of C. difficile. Thus, these results indicate that the coprisin analogue may prove useful as a therapeutic agent for C. difficile infection-associated inflammatory diarrhea and pseudomembranous colitis.
PMCID: PMC3186999  PMID: 21807975

Results 1-3 (3)