• Korean Journal of Poultry Science
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• v.35 no.4
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• pp.399-405
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• 2009

Two experiments were conducted to establish the basic data of feeding system in cross-bred Korean native chicks. A total of seven hundred twenty chicks were replaced the 36 floor pen for the first five weeks with $3{\times}3$ factorial design in Experiment 1. Four hundred eighty of five weeks old chicks were raised from six to ten weeks of age with $3{\times}2$ factorial design in Experiment 2. Dietary ME and CP were formulated to contain 3,000, 3,050, 3,100 kcal/kg and 21, 22, 23%, respectively in Experiment 1 and 3,050, 3,100, 3,150 kcal/kg and 18, 19% in Experiment 2. Weight gain, feed intake were measured and calculated the feed conversion. Blood were collected and analyzed at the end of experiments. In Experiment 1, weight gain showed significantly higher in 3,050, 3,100 kcal/kg treatments than 3,000 kcal/kg treatment (P<0.05), but was not different in CP treatments. Feed intake was statistically high in 3,000 kcal/kg treatment compared with 3,050 and 3,100 kcal/kg ones (P<0.05), and more increased in 21% CP treatments compared to that of 22 and 23 CP treatment (P<0.05). Feed conversion of birds fed 3,050 and 3,100 kcal/kg diet showed much lower than 3,000 kcal/kg treatments (P<0.05). FCR was signicantly improved (P<0.05) in chicks fed diets containing 21 and 22% CP as compared to that fed 20% CP. Blood protein, glucose, and total cholesterol tended to increase in high energy and diet treatments. Blood HDL was increased as dietary energy increased, whereas LDL increased in low CP treatments. In Experiment 2, weight gain was not consistent between treatments, but more increased in 18% CP treatments compared to that of 19% CP treatment from six to ten weeks old in cross bred chicks (P<0.05). Feed intake was similar to the result of weight gain, but more increased in 19% CP treatment than 18% CP treatment (P<0.05). There were no statistically difference in FCR, but seemed to improve as dietary ME increased. Blood total protein and glucose increased as dietary CP was high, but triglyceride and HDL increased in high versus low ME (P<0.05). The results of these experiments suggested that optimum dietary ME and CP, were 3,050, 3,150kcal/kg and 22, 19% for the first five weeks and second one, respectively.

• Korean Journal of Environmental Agriculture
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• v.28 no.2
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• pp.125-130
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• 2009

The aim of this study was to investigate whether differences in the distribution of soil invertebrates among different vegetation types (forest, reservoir, and crop land types) in rural area. A total of 18 orders and 137 species were collected by pitfall traps. Species numbers were the lowest (33 species) at the Chamaecyparis obtusa plantation (St. 6). On the forest sites, the individual number of Hymenoptera was the most abundant, and Acari and Coleoptera was the relatively more abundant than the other sites. On the reservoir sites (Salix chaenomeloides community), the individual number of Collembola was the most abundant, and Diptera was the relatively more abundant than the other sites. On the crop land sites, the individual numbers of Collembola, Hymenoptera, and Araneae were the relatively more abundant than the other orders. The density of Araneae was higher in the reservoir and crop land sites than in the forest sites. From a point of view of biodiversity, although the diversity index(H') was the highest in the mixed broad-leaved forest type (St. 2) with Quercus serrata and Q. acutissima, and the lowest in the upland levee of crop land(St. 11), there was no significant difference among the habitat or vegetation types. According to the community analysis, the soil invertebrates could be divided into 4 groups, the mixed broad-leaved forest type (A group), the plantation or pure forest type (B group), the reservoir type (C group), and the crop land type (D group).

• The Korean Journal of Pharmacology
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• v.25 no.1
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• pp.115-134
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• 1989

Combined effects of ganciclovir (GCV) and vidarabine (ara-A) on the replication, DNA synthesis, and gene expression of wild type-1 herpes simplex virus (HSV-1) and three acyclovir (ACV)-resistant HSV-1 mutants were studied. These mutants include a virus expressing no thymidine kinase $(ACV^r)$, a virus expressing thymidine kinase with altered substrate specificity $(IUdR^r)$, and a mutant expressing altered DNA polymerase $(PAA^r5)$. GCV, an agent activated by herpesvirus specific thymidine kinase, showed potent antiviral activity against the wild type HSV-1(KOS) and DNA polymerase mutant $(PAA^r5)$. The ACV-resistant mutants with thymidine kinase gene $(ACV^r\;and\;IUdR^r)$ were resistant to GCV. All tested wild type HSV-1 or ACV-resistant HSV-1 mutants did not display resistance to vidarabine (are-A). Combined GCV and ara-A showed potentiating synergistic antiviral activity against wild type KOS and $PAA^r5$, and showed subadditive combnined ativiral activity against thymidine kinase mutants. Combined GCV and ara-A more significantly inhibited the viral DNA synthesis in wild type KOS and $PAA^r5-infected$ cells to a greater extent than either agent alone, but the synergism was not determined in $ACV^r$ or $IUdR^r-infected$ cells. These data clearly indicate that combined GCV and ara-A therapy might be useful for the treatment of infections caused by wild type HSV-1 or ACV-resistant HSV-1 with DNA polymerase mutation. ACV-resistant viruses with the mutation in thymidine kinase gene are also, resistant to GCV, but susecptible to ara-A, indicating that ara-A would the drug of choice for the treatment of ACV-resistant HSV-1 which does not express thymidine kinase or expresses thymidine kinase with altered substrate specificity. While the synthesis of viral ${\alpha}-proteins$ of wild type HSV-1 was not affected by ACV, GCV, ara-A, or combined GCV and ara-A, the synthesis of ${\beta}-proteins$ was slightly but significantly increased at the later stage of viral infection by the antiviral agents. The synthesis of ${\gamma}-proteins$ of wild type HSV- 1 was significantly inhibited by ACV, GCV, ara-A, and combined GCV and ara-A. Combined GCV $(5-{\mu}M)$ and ara-A $(100-{\mu}M)$ also significantly altered the expression of viral ${\beta}-and$ ${\gamma}-proteins$, of which efffct was similar to that of GCV $(10-{\mu}M)$ alone. Although ACV at the concentration of $10-{\mu}M$ did not alter the expression of ${\alpha}-$, ${\beta}-$, and ${\gamma}-proteins$ of ACV-resistant $PAA^r5$, GCV and ara-A significantly alter the epression of ${\beta}-and$ ${\gamma}-proteins$, not ${\alpha}-protein$, as same manner as they altered the expression of those proteins in cells inffcted with wild type HSV-1. Combined GCV $(5-{\mu}M)$ and ara-A $(100-{\mu}M)$ altered the expression ${\beta}-and$ ${\gamma}-proteins$ in $PAA^r5$ infected cells, and the effect of combined regimen was comparable of that of GCV $(10-{\mu}M)$. These data indicate that the alteration in the expression of ${\beta}-and$ ${\gamma}-proteins$ in wild type HSV-1 or $PAA^r5$ infected cells could be more significantly affected by combined GCV and are-A than individual GCV or ara-A. In view of the fact that (a) viral ${\alpha}-$, ${\beta}-$, and ${\gamma}-proteins$ are synthesized in a cascade manner; (b) ${\beta}-proteins$ are essential for the synthesis of viral DNA; (c) the synthesis of ${\beta}-proteins$ are inhibited by ${\gamma}-proteins$; and (d) most ${\gamma}-proteins$ are made from the newly synthesized progeny virus, it is suggested that GCV and ara-A, alone or in combination, primarily inhibit the synthesis of viral DNA, and by doing so might exhibit their antiherpetic activity. The alteration in viral protein synthesis in the presence of tested antiviral agents could result from the alteration in viral DNA synthesis. From the present study, it can be concluded that (a) combined GCV and ara-A therapy would be beneficial for the control of inffctions caused by wild type HSV-1 or ACV-resistant DNA polymerase mutants; (b) the combined synergistic activity of GCV and ara-A is due to further decrease in the viral DNA by the combined regimen; (c) ara-A is the drug of choice for the infection caused by ACV-resistant HSV-1 with thymidine kinase mutation; and (d) the alteration in viral protein synthesis by GCV and ars-A, alone or in combination, is mostly due to the decreased synthesis of viral DAN.