Ho-Seong Cho

Electron capture behaviors of deep level traps in unintentionally doped and intentionally doped n-type GaN

In n-type GaN films grown on sapphire substrates by metal-organic chemical vapor deposition such as unintentionally GaN and intentionally Si-doped GaN and In-doped GaN, the electron capture behaviors were investigated by deep level transient spectroscopy with various filling pulse durations. Two distinct deep levels E1 and E2 were typically observed in unintentionally doped n-type GaN. After optimized growth of undoped GaN, deep level E1 disappears. With increasing Si doping, the trap concentration of deep level E2 is increased. However, In doping in n-type GaN growth was found to suppress the formation of deep level E2. The electrons captured at the traps E1 and E2 were found to depend logarithmically on the duration time of the filling pulse. From an analysis of a model involving barrier-limited capture rate, it can be concluded that deep level E1 is associated with linear line defects along dislocation cores while deep level E2 is related to point defects.

Molecular characterization of Aeromonas species isolated from farmed eels (Anguilla japonica).

Seventy Aeromonas strains were identified by phylogenetic analysis using housekeeping genes (gyrB and rpoD) in order to investigate etiological agents for aeromoniasis in farmed eels (Anguilla japonica). The phylogenetic analysis showed that Aeromonas aquariorum (n=22, 31.4%) was the predominant species among the investigated eel strains, followed by Aeromonas caviae (n=16, 22.9%), A. veronii (n=13, 18.6%), A. hydrophila (n=12, 17.1%), A. jandaei (n=4, 5.7%), A. media (n=2, 2.9%), and A. trota (n=1, 1.4%). The potential virulence of the present strains was estimated by performing PCR assays using the following seven virulence genes: cytotoxic enterotoxin (act), two cytotonic enterotoxins (alt and ast), glycerophospholipid:cholesterol acyltransferase (gcaT), DNase (exu), lipase (lip), and flagellin (fla). The detection rates of act, alt, ast, gcaT, exu, lip, and fla among all 70 strains were 91.4%, 55.7%, 27.1%, 97.1%, 95.7%, 100%, and 98.6%, respectively. In genotyping of enterotoxin genes, act(+)/alt(+)/ast(+), act(+)/alt(+)/ast(-), and act(+)/alt(-)/ast(-) genotypes were prevalent in A. hydrophila (8/12 strains), A. aquariorum (13/22 strains), and A. caviae (14/16 strains), respectively, suggesting a high heterogeneity among Aeromonas species. In this study, A. aquariorum, which has been an unrecorded species in Korea, can be an etiological agent for aeromoniasis of eel.

Upregulation of heme oxygenase-1 by ginsenoside Ro attenuates lipopolysaccharide-induced inflammation in macrophage cells.

Background The beneficial effects of ginsenoside species have been well demonstrated in a number of studies. However, the function of ginsenoside Ro (GRo), an oleanane-type saponin, has not been sufficiently investigated. Thus, the aim of the present study was to investigate the anti-inflammatory effects of GRo in vitro using the Raw 264.7 mouse macrophage cell line treated with lipopolysaccharide (LPS), and to clarify the possible mechanism of GRo involving heme oxygenase-1 (HO-1), which itself plays a critical role in self-defense in the presence of inflammatory stress. Methods Raw 264.7 cells were pretreated with GRo (up to 200μM) for 1 h before treatment with 1 μg/mL LPS, and both cell viability and inflammatory markers involving HO-1 were evaluated. Results GRo significantly increased cell viability in a dose dependent manner following treatment with LPS, and decreased levels of reactive oxygen species and nitric oxide. GRo decreased inflammatory cytokines such as nitric oxide synthase and cyclooxygenase-2 induced by LPS. Moreover, GRo increased the expression of HO-1 in a dose dependent manner. Cotreatment of GRo with tin protoporphyrin IX, a selective inhibitor of HO-1, not only inhibited upregulation of HO-1 induced by GRo, but also reversed the anti-inflammatory effect of GRo in LPS treated Raw 264.7 cells. Conclusion GRo induces anti-inflammatory effects following treatment with LPS via upregulation of HO-1.

The Prevalence of Coxiella burnetii Infection in Wild Korean Water Deer, Korea

ABSTRACT The aim of this study was to evaluate the prevalence of Coxiella burnetti infection in wild Korean water deer (Hydropotes inermis argyropus) in Korea, by using serology and real-time PCR analyses. One hundred ninety-six sera were collected from 4 provinces and tested for anti-C. burnetii antibody detection, by means of CHEKIT Q fever ELISA kit; and C. burnetii IS1111 insertion sequence detection, by means of real-time PCR. Antibodies were detected in 18 of the 196 (9.18%) serum samples, whereas genomes of C. burnetii were detected in 13 of the 196 (6.63%) serum samples. Based on overall high seroprevalence, the public health implications of these findings are important, because they indicate that asymptomatic seropositive or seronegative wild animals may be consistently shedding C. burnetii. This is the first study of C. burnetii prevalence in Korean water deer in the Republic of Korea that has indicated the presence of infected animals throughout the country.

Arsenite Acutely Decreases Nitric Oxide Production via the ROS-Protein Phosphatase 1-Endothelial Nitric Oxide Synthase-Thr 497 Signaling Cascade

Chronic (>24 h) exposure of arsenite, an environmental toxicant, has shown the decreased nitric oxide (NO) production in endothelial cells (EC) by decreasing endothelial NO synthase (eNOS) expression and/or its phosphorylation at serine 1179 (eNOS-Ser1179 in bovine sequence), which is associated with increased risk of vascular diseases. Here, we investigated the acute (<24 h) effect of arsenite on NO production using bovine aortic EC (BAEC). Arsenite acutely increased the phosphorylation of eNOS-Thr497, but not of eNOS-Ser116 or eNOS-Ser1179, which was accompanied by decreased NO production. The level of eNOS expression was unaltered under this condition. Treatment with arsenite also induced reactive oxygen species (ROS) production, and pretreatment with a ROS scavenger N-acetyl-L-cysteine (NAC) completely reversed the observed effect of arsenite on eNOS-Thr497 phosphorylation. Although protein kinase C (PKC) and protein phosphatase 1 (PP1) were reported to be involved in eNOS-Thr497 phosphorylation, treatment with PKC inhibitor, Ro318425, and overexpression of various PKC isoforms did not affect the arsenite-stimulated eNOS-Thr497 phosphorylation. In contrast, treatment with PP1 inhibitor, calyculin A, mimicked the observed effect of arsenite on eNOS-Thr497 phosphorylation. Lastly, we found decreased cellular PP1 activity in arsenite-treated cells, which was reversed by NAC. Overall, our study demonstrates firstly that arsenite acutely decreases NO production at least in part by increasing eNOS-Thr497 phosphorylation via ROS-PP1 signaling pathway, which provide the molecular mechanism underlying arsenite-induced increase in vascular disease.

The Green Tea Component (-)-Epigallocatechin-3-Gallate Sensitizes Primary Endothelial Cells to Arsenite-Induced Apoptosis by Decreasing c-Jun N-Terminal Kinase-Mediated Catalase Activity.

The green tea component (-)-epigallocatechin-3-gallate (EGCG) has been shown to sensitize many different types of cancer cells to anticancer drug-induced apoptosis, although it protects against non-cancerous primary cells against toxicity from certain conditions such as exposure to arsenic (As) or ultraviolet irradiation. Here, we found that EGCG promotes As-induced toxicity of primary-cultured bovine aortic endothelial cells (BAEC) at doses in which treatment with each chemical alone had no such effect. Increased cell toxicity was accompanied by an increased condensed chromatin pattern and fragmented nuclei, cleaved poly(ADP-ribose) polymerase (PARP), activity of the pro-apoptotic enzymes caspases 3, 8 and 9, and Bax translocation into mitochondria, suggesting the involvement of an apoptotic signaling pathway. Fluorescence activated cell sorting analysis revealed that compared with EGCG or As alone, combined EGCG and As (EGCG/As) treatment significantly induced production of reactive oxygen species (ROS), which was accompanied by decreased catalase activity and increased lipid peroxidation. Pretreatment with N-acetyl-L-cysteine or catalase reversed EGCG/As-induced caspase activation and EC toxicity. EGCG/As also increased the phosphorylation of c-Jun N-terminal kinase (JNK), which was not reversed by catalase. However, pretreatment with the JNK inhibitor SP600125 reversed all of the observed effects of EGCG/As, suggesting that JNK may be the most upstream protein examined in this study. Finally, we also found that all the observed effects by EGCG/As are true for other types of EC tested. In conclusion, this is firstly to show that EGCG sensitizes non-cancerous EC to As-induced toxicity through ROS-mediated apoptosis, which was attributed at least in part to a JNK-activated decrease in catalase activity.

Aeromonas hydrophila-Associated Septicemia in Captive Crocodiles (Crocodylus johnstoni and Crocodylus porosus)

Abstract: Five 25-yr-old crocodiles (Crocodylus johnstoni and Crocodylus porosus) were diagnosed with Aeromonas hydrophila–associated septicemia accelerated by improper thermoregulation. At necropsy, pulmonary congestion and pleural effusion were the main lesions in the thorax. Necrotizing enteritis, intestinal hemorrhage, fibrinous serositis, hepatitis, and pancreatitis were observed in the abdominal cavities of all five crocodiles. Aeromonas hydrophila was identified in the pleural effusions and abdominal ascites of all necropsied crocodiles by using an API system 20NE. Aeromonas hydrophila infection and evaluation of virulence were confirmed by polymerase chain reaction targeting the 16S rRNA and extracellular hemolysin gene. The crocodiles in the present case were housed in an indoor facility at a private zoo that failed to optimize land and water portions of the enclosure, exposing the animals to impeded thermoregulation, and it is suggested that the pathogenesis was accelerated by the improper thermoregulation-induced stress. This is the first description of A. hydrophila pathogenicity associated with impeded thermoregulation in reptiles.

Direct measurement of electron transport in GaN/sapphire interface layer grown by metalorganic chemical vapor deposition

Hall effect and capacitance–voltage measurements confirm a conductive thin layer near the GaN/sapphire interface. The temperature-dependent Hall effect of the interface layer was directly measured at temperatures above 100 K, and the results were satisfactorily described by solving the Boltzmann transport equation with various scattering mechanisms. Transport occurs in the conduction band of the layer and is characterized by two dominant scattering mechanisms due to space charge and ionized impurity. The high acceptor density and large space charge effect are related with the dislocations in the interface layer.

Evaluation of two commercial PRRSV antibody ELISA kits with samples of known status and singleton reactors.

Two commercial PRRSV ELISA kits (IDEXX and Bionote) were evaluated for their sensitivity and specificity using 476 PRRS-positive serum samples collected from 7 animal challenge experiments and 1,000 PRRS-negative sera. Both ELISA kits exhibited 100% sensitivity with sera collected 14 to 42 days post-infection, and the results from the kits were highly correlated (R2=0.9207). The specificity of IDEXX or Bionote kit was 99.9% or 99.7%, respectively. In addition, the Bionote ELISA kit was used to examine 100 sera that were determined to be falsely positive either by IDEXX 2XR or 3XR ELISA, and only 7 of these samples were found to be positive. These results indicate that both ELISA kits exhibited similar levels of sensitivity and specificity and would complement one another for the verification of false-positive samples.

Effect of isoelectronic In doping on deep levels in GaN grown by MOCVD

We have investigated the effect of isoelectronic In doping on deep levels in GaN films grown by metalorganic chemical vapor deposition via deep level transient spectroscopy. Deep level E2 0.5 eV below the conduction band was observed in both undoped GaN and In-doped GaN. However, with increasing In mole flow rate, the trap concentration of E2 decreases sharply from 2.3 × 10 14 to 2.27 × 10 13 cm -3 , nearly an order of magnitude in reduction, comparing to undoped GaN. This might be due to the dislocation pinning and/or bending effect. Therefore, In doping in GaN growth can effectively decrease the dislocation density and suppress the formation of deep levels E2.