Young Hee Lim

Viral etiology and incidence associated with acute gastroenteritis in a 5-year survey in Gyeonggi province, South Korea

BACKGROUND Acute gastroenteritis caused by viruses is one of the leading causes of childhood morbidity. OBJECTIVE The incidence and etiology of virus-associated gastroenteritis during 2001-2005 in Gyeonggi province, South Korea was determined. STUDY DESIGN A total of 10,028 stool specimens were analyzed with enzyme immunoassay, reverse transcription-polymerase chain reaction, and nucleotide sequencing. Phylogenetic analysis of genotype sequences was performed for each of four commonly detected viral pathogens. RESULTS At least one viral agent was detected in 29.0% (2908 of 10,028) of the stool samples. Among these, rotavirus was most numerous (66.7%) followed by norovirus (12.6%), astrovirus (11.9%), and enteric adenovirus (2.6%). Mixed infections were identified in 180 cases (1.8%). Patients aged 1-5 years had the largest proportion 83.6% (2430 of 2908) of virus-positive stool specimens. Viral-mediated gastroenteritis was most common from December to May. The most prevalent strains of rotavirus, adenovirus, astrovirus, and norovirus were G1 type, type 41, G1 type, and GII-1 type, respectively. CONCLUSIONS Our finding showed the diversity of viral causative agents of gastroenteritis and the prevalence of each gastroenteritis-associated viral genotype in South Korea.

Resveratrol antibacterial activity against Escherichia coli is mediated by Z-ring formation inhibition via suppression of FtsZ expression

Resveratrol exhibits a potent antimicrobial activity. However, the mechanism underlying its antibacterial activity has not been shown. In this study, the antibacterial mechanism of resveratrol was investigated. To investigate induction of the SOS response, a strain containing the lacZ+gene under the control of an SOS-inducible sulA promoter was constructed. DNA damage was measured by pulse-field gel electrophoresis (PFGE). After resveratrol treatment, the cells were observed by confocal microscopy. For the RNA silencing assay, ftsZ-specific antisense peptide nucleic acid (PNA) was used. Reactive oxygen species (ROS) production increased in Escherichia coli after resveratrol treatment; however, cell growth was not recovered by ROS quenching, indicating that, in this experiment, ROS formation and cell death following resveratrol treatment were not directly correlated. Resveratrol treatment increased DNA fragmentation in cells, while SOS response-related gene expression levels increased in a dose-dependent manner. Cell elongation was observed after resveratrol treatment. Elongation was induced by inhibiting FtsZ, an essential cell-division protein in prokaryotes, and resulted in significant inhibition of Z-ring the formation in E. coli. The expression of ftsZ mRNA was suppressed by resveratrol. Our results indicate that resveratrol inhibits bacterial cell growth by suppressing FtsZ expression and Z-ring formation.

Inhibitory effect of mulberroside A and its derivatives on melanogenesis induced by ultraviolet B irradiation.

Mulberroside A was isolated from the ethanol extract of Morus alba roots. The enzymatic hydrolysis of mulberroside A with Pectinex produced oxyresveratrol and oxyresveratrol-3-O-glucoside. We tested oxyresveratrol, oxyresveratrol-3-O-glucoside, and mulberroside A to determine whether they could inhibit ultraviolet B (UVB) irradiation-induced melanogenesis in brown guinea pig skin. Topical application of mulberroside A, oxyresveratrol, and oxyresveratrol-3-O-glucoside reduced the pigmentation in guinea pig skin. These compounds suppressed the expression of melanogenic enzymes tyrosinase, tyrosinase-related protein-1, and microphthalmia transcription factor. The anti-melanogenesis effect was highest with oxyresveratrol, intermediate with oxyresveratrol-3-O-glucoside, and lowest with mulberroside A. Mulberroside A is a glycosylated stilbene of oxyresveratrol; thus, the deglycosylation of mulberroside A resulted in enhanced inhibition of melanogenesis. Histological analysis with Fontana-Masson staining confirmed that these compounds significantly reduced the melanin content in the epidermis of UVB-irradiated guinea pig skin compared to the vehicle control. Thus, these compounds effectively reduced pigmentation and may be suitable cosmetic agents for skin whitening.

Genotypic distribution of rotavirus strains causing severe gastroenteritis in Gyeonggi province, South Korea, from 2003 to 2005

Rotavirus was present in 1,367 of 7,060 stool samples (19.4%) collected in Gyeonggi province of South Korea from 2003 through 2005. The predominant genotypes were confirmed as G4/P2A[6] (19.0%) followed by G3/P1A[8] (15.6%), G2/P1B[4] (9.3%), and G1/P1A[8] (6.5%). The predominant types of rotavirus by year were G3/P[8] in 2003, G4/P[6] in 2004, and G1/P[8] in 2005. The prevalent rotavirus genotypes changed constantly from 2003 to 2005.

A survey of intestinal protozoan infections among gastroenteritis patients during a 3-year period (2004-2006) in Gyeonggi-do (Province), South Korea

The incidence and etiology of parasite-associated gastroenteritis during 2004-2006 in Gyeonggi-do (province), South Korea was determined by means of antigen detection ELISA on 6,071 stool specimens collected from 6 general hospitals. At least 1 parasitic agent was detected in 3.4% (208/6,071) of the stool samples. Among these, Giardia lamblia was the most numerous (152 cases; 2.5%), followed by Entamoeba histolytica (25 cases; 0.4%), Cryptosporidium parvum (23 cases; 0.4%), and mixed infections (8 cases; 0.1%). Patients aged 1-5 years had the largest proportion (69.2%; 144/208) of parasite-positive stool specimens. Parasite-mediated gastroenteritis was most common from June to September. The detection rate gradually increased from 2004 to 2006. This study shows that parasite-mediated gastroenteritis may be significant among children in Korea and that parasite infection surveillance should be constantly performed.

Dairy Propionibacterium extends the mean lifespan of Caenorhabditis elegans via activation of the innate immune system.

Dairy Propionibacterium freudenreichii is a candidate non-lactic acid probiotic. However, little information is available on the effect of P. freudenreichii on lifespan extension in humans. The aim of this study was to evaluate the effects of P. freudenreichii on lifespan extension and to elucidate the mechanism of P. freudenreichii-dependent lifespan extension in Caenorhabditis elegans. The results showed that P. freudenreichii significantly (p < 0.05) extended the lifespan of C. elegans compared with Escherichia coli OP50, a standard food for the worm. Analysis of age-related biomarkers showed that P. freudenreichii retards ageing. Moreover, P. freudenreichii increased resistance against a human pathogen, Salmonella typhimurium, through the activation of skn-1, which is involved in pathogen resistance in C. elegans. Furthermore, P. freudenreichii-fed daf-16, jnk-1, skn-1 or daf-7 loss-of-function mutants showed an extended mean lifespan compared with E. coli OP50-fed worms. However, the increase in lifespan was not observed in pmk-1, sek-1, mek-1, dbl-1, daf-12 or daf-2 mutants, which suggests potential roles for these genes in P. freudenreichii-induced longevity in C. elegans. In conclusion, P. freudenreichii extends the lifespan of C. elegans via the p38 MAPK pathway involved in stress response and the TGF-β pathways associated with anti-inflammation processes in the immune system.

Elucidating the Mechanism of Weissella-dependent Lifespan Extension in Caenorhabditis elegans

The mechanism whereby lactic acid bacteria extend the lifespan of Caenorhabditis elegans has previously been elucidated. However, the role of Weissella species has yet not been studied. We show that Weissella koreensis and Weissella cibaria significantly (p < 0.05) extend the lifespan of C. elegans compared with Escherichia coli OP50 and induce the expression of several genes related to lifespan extension (daf-16, aak-2, jnk-1, sod-3 and hif-1). Oral administration of Weissella altered reactive oxygen species (ROS) production and lowered the accumulation of lipofuscin and increased locomotor activity (which translates to a delay in ageing). Moreover, Weissella-fed C. elegans had decreased body sizes, brood sizes, ATP levels and pharyngeal pumping rates compared with E. coli OP50-fed worms. Furthermore, mutations in sod-3, hif-1 or skn-1 did not alter lifespan extension compared with wild-type C. elegans. However, C. elegans failed to display lifespan extension in loss-of-function mutants of daf-16, aak-2 and jnk-1, which highlights the potential role of these genes in Weissella-induced longevity in C. elegans. Weissella species extend C. elegans lifespan by activating DAF-16 via the c-Jun N-terminal kinase (JNK) pathway, which is related to stress response, and the AMP-activated protein kinase (AMPK)-pathway that is activated by dietary restriction.

Antihyperlipidemic Effects of Rhapontin and Rhapontigenin from Rheum undulatum in Rats Fed a High-Cholesterol Diet

Rhapontin was purified from a methanol extract from the roots of Rheum undulatum, and rhapontigenin was produced by an enzymatic transformation of rhapontin. Rats were fed a high-cholesterol diet to induce hyperlipidemia, followed by oral treatment with rhapontin or rhapontigenin (1-5 mg/kg/day). Rhapontin and rhapontigenin treatment resulted in a significant (p<0.05) dose-dependent decrease in the serum lipid level, while the high-density lipoprotein cholesterol level increased slightly compared with the experimental control. Furthermore, rhapontin and rhapontigenin treatment improved the pathological characteristics of the degenerating fatty liver in high-cholesterol diet-induced hyperlipidemic rats dose-dependently. Aspartate aminotransferase and alanine aminotransferase levels in rhapontin- and rhapontigenin-treated hyperlipidemic rats were not significantly different from those in the control. These results indicate that rhapontin and rhapontigenin can be used as potent antihyperlipidemic agents.

Evaluation of the inhibition of mushroom tyrosinase and cellular tyrosinase activities of oxyresveratrol: comparison with mulberroside A.

The inhibitory effects of oxyresveratrol, the aglycone of mulberroside A, on mushroom and cellular tyrosinase activities and melanin synthesis were evaluated. Mulberroside A and oxyresveratrol showed inhibitory activity against mushroom tyrosinase, with oxyresveratrol demonstrating a greater inhibitory effect than that of mulberroside A. Oxyresveratrol and mulberroside A strongly inhibited melanin production in Streptomyces bikiniensis and exhibited dose-dependent inhibition of tyrosinase activity and inhibition of melanin synthesis in B16F10 melanoma cells. However, the compounds exhibited nearly similar inhibitory effects on the activity of cellular tyrosinase and melanin synthesis in murine melanocytes. The inhibition of melanin synthesis by mulberroside A and oxyresveratrol was involved in suppressing the expression level of melanogenic enzymes, tyrosinase, tyrosinase-related protein-1 (TRP-1), and tyrosinase-related protein-2 (TRP-2). These results indicate that the inhibition rate of mushroom tyrosinase might not provide an accurate estimate of the inhibition rate of melanin synthesis in melanocytes.

Brief Communication: SIR-2.1-dependent lifespan extension of Caenorhabditis elegans by oxyresveratrol and resveratrol

Resveratrol (RES) has been studied for its effects on the lifespan extension of Caenorhabditis elegans, but controversy still remains on its mechanism related with SIR-2. In this study, longevity assay was performed to confirm SIR-2-dependent lifespan extension of C. elgeans with RES and oxyresveratrol (OXY), an isomer of hydroxylated RES using loss-of-function mutants of C. elegans including sir-2.1 mutant. The results showed that OXY and RES significantly (P < 0.05) extended the lifespan of C. elegans compared with the control. OXY and RES also significantly (P < 0.05) increased the mRNA expression levels of sir-2.1 and aak-2 in a dose-dependent manner and increased the protein expression levels of SIR-2.1. OXY and RES treatment extended the lifespan in daf-16 loss-of-function mutants, which suggested that lifespan extension was not occurring via the activation of DAF-16. However, OXY and RES failed to extend the lifespan in loss-of-function mutants of sir-2.1 and aak-2. Therefore, OXY and RES extend the lifespan of C. elegans by overexpression of SIR-2.1, which is related to lifespan extension through calorie restriction and the AMP-activated protein kinase (AMPK) pathway, although this process is independent of the FOXO/DAF-16 pathway.