• Korean Journal of Environmental Agriculture
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• v.12 no.2
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• pp.153-161
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• 1993

This study was conducted to compare the resistance and sensitivity of trees with 6 native species exposing to 4 different levels of $SO_2$gas(0.4, 0.7, 1.5 and 3.0 ppm) respectively. The results are summarized as follows : 1. Visible injuries appeared as spots in the region of intervein on the leaves for all the species and the color of the spots changed from light green and/or brown to light brown, dark brown, and/or redish brown. 2. The sensitivity of the species to $SO_2$ was high in the descending order of Zizyphus jujuba, Cataegus pinnatifida, Viburnum sargentii, Weigela subsessilis, Euonymus japonica, and Acer ginnala. 3. The resistance of the species to $SO_2$ was high in the descending order of Acer ginnala, Eunymus japonica Viburnum sargentii, Weigela subsessilis, Zizyphus jujuba, and Crataegus pinnatifida. 4. When the trees were exposed to $SO_2$gas, the contents of chlorophyll a, b, and a+b were consostently lower than those of control, and water soluble sulfur contents in the leaves were higher than those of control. 5. There was no significant correlation between stomatal resistance and the sensitivity(or resistance) of the trees exposed to $SO_2$ gas. 6. In this study, it was concluded that Acer ginnala was more suitable species than the others for landscape in air polluted area because it showed high resistance, low sensitivity, and low stromal resistance to $SO_2$gas exposure.

• 한국환경농학회:학술대회논문집
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• 2009.07a
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• pp.273-282
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• 2009

The transmissible spongiform encephalopathies (TSEs) disease group are fatal neurodegenerative disorders affecting a wide range of hosts. The group includes kuru and Creutzfeldt-Jakob disease (CJD) in humans, scrapie in sheep and goats and Bovine spongiform encephalopathy (BSE) in cattle. The exact nature of the infectious agent involved in the transmission of these diseases remains controversial. However, a central event in their pathogenesis is the accumulation in infected tissues of an abnormal form of a host-encoded protein, the prion protein (PrP). Whereas the normal cellular protein is fully sensitive to protease ($PrP^{sen}$), the disease-associated prion protein ($PrP^d$) is only partly degraded ($PrP^{res}$), its amino-terminal end being removed. BSE was first reported in the mid-80s in the UK. Ten years later, a new form of human prion disease, variant CJD (vCJD) developed in the wake of the BSE epidemic, and there is now strong scientific evidence that vCJD was initiated by the exposure of humans to BSE-infected tissues, thus indicating a zoonotic disease. However, the ban on the feeding of animal-derived proteins to ruminants, and the apparent lack of vertical transmission of BSE, have led to a decline in the incidence of the disease within cattle herd and therefore, an assumed decreased risk for human contacting vCJD. The origin of the original case(s) of BSE still remains an enigma even though three hypotheses have been raised. Hypotheses are i) sheep- or goat-derived scrapie-infected tissues included in meat and bone meal fed to cattle, ii) a previously undetected sporadic or genetic bovine TSE contaminating cattle feed or iii) originating from a human TSE through animal feed contaminated with human remains. A host cellular membrane protein ($PrP^C$), which is abundant in central nervous system tissue, appear to be conformationally altered in the diseased host into a prion protein ($PrP^{Sc}$). This $PrP^{Sc}$ is detergent insoluble and partially protease-resistant ($PrP^{res}$). The term $PrP^{res}$ is normally used to describe the protein detected after protease treatment, in techniques such as Western immunoblotting, and enzyme-linked immunosorbant assay using fresh/frozen tissue. Immunohistochemistry may performed with formalin-fixed tissues. Also, clinical signs of the BSE are one of the major diagnostic indicators. Recently, atypical forms (known as H- and L-type) of BSE have appeared in several European countries, Japan, Canada and the United States. An unusual case was also reported in a miniature zebu. The atypical BSE fall into two groups based on the relative molecular mass (Mm) of the unglycosylated $PrP^{res}$ band relative to that of classical BSE, one of the higher Mm (H-type) and the other lower (L-type). Both types have been detected worldwide as rare cases in older animals, at a low prevalence consistent with the possibility of sporadic forms of prion diseases in cattle. This raises the unwelcome possibility that vCJD could increase in the human population. Now, active surveillance program against BSE is going on in Korea. In regional veterinary service lab, ELISA is applied to screen the BSE in slaughter and confirmatory tests by Western immunoblotting and immunohistochemisty are carried out if there are positive or suspect in the screening test. Also, the ruminant feed ban is rigorously enforced. Removal of specified risk materials such as brain and spinal cord from cattle is mandatory process at slaughter to prevent the infected material from entering the human food chain.

• Journal of Sericultural and Entomological Science
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• v.18 no.2
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• pp.83-88
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• 1976

A study was made on the interstrain difference in dose-infection response and induction response of silkworm to the two strains of cytoplasmic polyhedrosis virus to obtain some informations on screening the leading strains. Comparison of dose-infection responses of larvae following the inoculation of the inclusion body of cytoplasmic polyhedrosis virus revealed that there is no significance in the resistance to dose-infection and any of strains were more resistant at advanced stage(4th instar) than younger stage(2nd instar). In the pathogenicity between cytoplasmic polyhedrosis virus with hexagonal and tetragonal outline, the hexagonal polyhedra showed higher pathogenicity than the tetragonal polyhedra. However, the averages of $LC_{50}$ of cytoplasmic polyhedrosis virus with hexagonal outline to larvae of parental inbred line were 6.12${\times}$10$\^$6//$m\ell$ at 2nd instar and 1.57${\times}$10$\^$7//$m\ell$ at 4th instar in spring and those to their hybrids were 1.28${\times}$10$\^$6//$m\ell$ at 2nd ins tar and 4.99${\times}$10$\^$6//$m\ell$ at 4th ins tar in autumn. Meanwhile the $LC_{50}$ averages of tetragonal polyhedra. to larvae of parental inbred line were 2.06${\times}$10$\^$7//$m\ell$ at 2nd instar and 5.67${\times}$10$\^$7//$m\ell$ at 4th instar in spring and those to their hybrids were 9.84${\times}$10$\^$6//$m\ell$ at 2nd instar and 3.86${\times}$10$\^$7//$m\ell$ at 4th instar in autumn, respectively. In comparison of induction response of silkworm larvae to inoculation of tetragonal polyhedra of cytoplasmic polyhedrosis virus, the induction rate of hexagonal polyhedra was remarkably higher in the treatment of inoculation at 2nd instar than at 4th instar and at the concentration of 1.3${\times}$10$\^$6//$m\ell$ than at any others. Most of induction showed a mixed infection with hexagonal and tetragonal polyhedra of cytoplasmic polyhedrosis virus.

• Journal of Life Science
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• v.15 no.3 s.70
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• pp.415-422
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• 2005

library of the mutants was prepared by transposon mutagenesis of the Mycobacterium bovis BCG. We screened this library for the resistance to an anti-tuberculosis antibiotic, PA-824. Most of the mutants resistant to the PA-824 were not able to synthesize the coenzyme $F_{420}$ which is normally produced by the wild type M. bovis BCG strains. HPLC analysis of the cellular extract showed that one of those mutants which lost the ability to synthesize $F_{420}$ still produced F0. The insertion site of the transposon in this mutant was determined by an inverse PCR and the transposon was found to be inserted in the Rv2435c open reading frame (ORF). Rv2435c ORF is predicted to encode an 80.3 kDa protein. Rv2435c protein appears to be bound to the cytoplasmic membrane, its N-terminal present in the periplasm and C-terminal in the cytoplasm. The C-terminal portion of this protein is highly homologous with the adenylyl cyclases of both prokaryotes and eukaryotes. There are 15 ORFs which have homology with the class III AC proteins in the genome of the M. tuberculosis and M. bovis. Two of those, Rv1625c and Rv2435c, are highly homologous with the mammalian ACs. We cloned the cytoplasmic domain of the Rv2435c ORF and expressed it with six histidine residues attached on its C-terminal in Escherichia coli to find out if this protein is a genuine AC. Production of that protein in E. coli was proved by purifying the histidine-tagged protein by using the Ni-NTA resin. This protein, however, failed to complement the cya mutation in E. coli, indicating that this protein lacks the AC activity. All of the further attempts to convert this protein to a functional AC by a mutagenesis with UV or hydroxylamine, or construction of several different fusion proteins with Rv1625c failed. It is, therefore, possible that Rv2435c protein might affect the conversion of F0 to $F_{420}$ not by synthesizing cAMP but by some other way.

• Journal of Life Science
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• v.17 no.10
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• pp.1447-1451
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• 2007

Through the screening of marine natural compounds that inhibit cancer cell proliferation, we previously reported that pectenotoxin-2 (PTX-2) isolated from marine sponges exhibits selective cytotoxicity against several cell lines in p53-deficient tumor cells compared to those with functional p53. However, the molecular mechanisms of its anti-proliferative action on malignant cell growth are not completely known. To further explore the mechanisms of its anti-cancer activity and to test whether the status of p53 in liver cancer cells correlates with their chemo-sensitivities to PTX-2, we used two well-known hepatocarcinoma cell lines, p53-deficient Hep3B and p53-wild type HepG2. We have demonstrated that PTX-2 markedly inhibits Hep3B cell growth and induces apoptosis whereas HepG2 cells are much more resistant to PTX-2 suggesting that PTX-2 seems to act by p53-independent cytotoxic mechanism. The apoptosis induced by PTX-2 in Hep3B cells was associated with the modulation of DNA fragmentation factor (DFF) family proteins, up-regulation of pro-apoptotic Bcl-2 family members such as Bax and Bcl-xS and activation of caspases (caspase-3, -8 and -9). Blockade of the caspase-3 activity by caspase-3 inhibitor, z-DEVD-fmk, prevented the PTX-2-induced growth inhibition in Hep3B cells. Moreover, treatment with PTX-2 also induced phosphorylation of AKT and extracellular-signal regulating kinase (ERK), but not c-Jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (MARK). Specific inhibitors of PI3K inhibitor (LY294002) and ERK1/2 inhibitor (PD98059) significantly blocks PTX-2-induced-anti-proliferative effects, whereas a JNK inhibitor (SP600125) and a p38 MAPK inhibitor (SB203580) have no significant effects demonstrating that the pro-apoptotic effect of PTX-2 mediated through activation of AKT and ERK signal pathway in Hep3B cells.