• Korean Journal of Fisheries and Aquatic Sciences
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• v.17 no.6
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• pp.511-522
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• 1984

The Nagdong is one of the biggest rivers in Korea, which is very important water source not only for tap water of Pusan city but also for the industrial water. Therefore, authors tried to check the water quality year by year. In this experiment one hundred and twenty water samples collected from August 1983 to July 1984 were analyzed bacteriologically and physiologically. Fifteen sampling stations were established between near Samrangjin and estuary of the river. To evaluate the water quality, temperature, pH, chloride ion, salinity, chemical oxygen demand (COD), electrical conductivity, nutrients, total coliform, fecal coliform, fecal streptococcus, viable cell count and bacterial flora were observed. The variation of water temperature was ranged $-1.5{\sim}29.0^{\circ}C$ (Mean value $13.9{\sim}16.5^{\circ}C$), it in spring was higher as $10{\sim}15^{\circ}C$ about $10^{\circ}C$ than in winter and it in autumm was very stabilized as about $20^{\circ}C$ at each station. The pH variation of the samples was ranged $6.68{\sim}9.15$. The range of concentration of chloride ion and salinity varied $7.4{\sim}l,020.5$ mg/l and $1.05{\sim}33.0\%0$, respectively. Especially, salinity of the 3rd water war was the higher than others as $25.76{\sim}31.58\%0$. COD was ranged $1.45{\sim}14.94$ mg/l and the lower part of the Nagdong River was heavily contaminated by domesitc sewage and waste water from the adjacent factor area. The range of electrical conductivity was $1.360{\times}10^2{\sim}5.650{\times}10^4{\mu}{\mho}/cm$ and that was by far higher the estuary than the upper. Concentration of nutrients were $0.008{\sim}0.040$ mg/l (Mean value $0.019{\sim}0.068$ mg/l) for $NO_2-N,\;0.038{\sim}5.253$ mg/l ($0.351{\sim}2.347$ mg/l) for $NO_3-N,\;0.100{\sim}2.685$ mg/l($0.117{\sim}1.380$ mg/l) for $NH_4-N,\;0.003{\sim}0.084$ mg/l($0.014{\sim}0.065$ mg/l) for $PO_4-P$ and $0.154{\sim}6.123$ mg/l ($1.165{\sim}3.972$ mg/l) for $SiO_2-Si$, respectively. Usually nutrients contents of the water in the upper part(included station 1 to 5) were higher than those of the estuarine area. The bacterial density of the samples ranged 7.3 to 460,000/100 ml for total coliforms, 3.6 to 460,000/100 ml for fecal coliform, $0{\sim}46,000/100ml$ for fecal streptococcus and $<30{\sim}1.2{\times}10^5/ml$ for viable cell count. Composition of coliform was $28\%$ Escherichia coli group, $18\%$ Citrobacter freundii group, $31\%$ Enterobacter aerogenes group and $22\%$ others. Predominant species among the 659 strains isolated from the samples were Pseudomonas spp. ($42\%$), Flavobacterium spp. ($20\%$) and Moraxella spp. ($12\%$).

• Economic and Environmental Geology
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• v.8 no.3
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• pp.117-124
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• 1975

Wet chemical analysis (for $MnO_2$, MnO, and $H_2O$(+)) and electron microprobe analysis (for $Fe_2O_3$ and PbO) give $MnO_2$ 74.91, MnO 11.33, $Fe_2O_3$ (total Fe) 4.19, PbO 0.03, $H_2O$ (+) 9.46, sum 99.92%. 'Available oxygen determined by oxalate titration method is allotted to $MnO_2$ from total Mn, and the remaining Mn is calculated as MnO. Traces of Ba, Ca, Mg, K, Cu, Zn, and Al were found. Li and Na were not found. The existence of (OH) is verified from the infrared absorption spectra. The analysis corresponds to the formula $Mn^{4+}{_{4.85}}(Mn^{2+}{_{0.90}}Fe^{3+}{_{0.30}})_{1.20}O_{8.09}(OH)_{5.91}$, on the basis of O=14, 'or ideally $Mn^{4+}{_{5-x}}(Mn^{2+},Fe^{3+})_{1+x}O_{8}(OH)_{6}$ ($x{\approx}0.2$). X-ray single crystal study could not be made because of the distortion of single crystals. But the x-ray powder pattern is satisfactorily indexed by an orthorhombic cell with a 9.324, b 14.05, c $7.956{\AA}$., Z=4. The indexed powder diffraction lines are 9.34(s) (100), 7.09(s) (020), 4.62(m) (200, 121), 4.17(m) (130), 3.547(s) (112), 3.212(vw) (041), 3.101(s) (300), 2.597(w) (013), 2.469(m) (331), 2.214(vw)(420), 2.098(vw) (260), 2.014 (vw) (402), 1.863(w) (500), 1.664(w) (314), 1.554(vw) (600), 1.525(m) (601), 1.405(m) (0.10.0). DTA curve shows the endothermic peaks at $250-370^{\circ}C$ and $955^{\circ}C$. The former is due to the dehydration: and oxidation forming$(Mn,\;Fe)_2O_3$(cubic, a $9.417{\AA}$), and the latter is interpreted as the formation of a hausmannite-type oxide (tetragonal, a 5.76, c $9.51{\AA}$) from $(Mn,\;Fe)_2O_3$. Infrared absorption spectral curve shows Mn-O stretching vibrations at $515cm^{-1}$ and $545cm^{-1}$, O-H bending vibration at $1025cm^{-1}$ and O-H stretching vibration at $3225cm^{-1}$. Opaque. Reflectance 13-15%. Bireflectance distinct in air and strong in oil. Reflection pleochroism changes from whitish to light grey. Between crossed nicols, color changes from yellowish brown with bluish tint to grey in air and yellowish brown to grey through bluish brown in oil. No internal reflections. Etching reactions: HCl(conc.) and $H_2SO_4+H_2O_2$-grey tarnish; $SnCl_2$(sat.)-dark color; $HNO_3$(conc.)-grey color; $H_2O_2$-tarnish with effervescence. It is black in color. Luster dull. Cleavage one direction perfect. Streak brownish black to dark brown. H. (Mohs) 2-3, very fragile. Specific gravity 3.59(obs.), 3.57(calc.). It occurs as radiating groups of flakes, flower-like aggregates, colloform bands, dendritic or arborescent masses composed of fine grains in the cementation zone of the supergene manganese oxide deposits of the Janggun mine, Bonghwa-gun, southeastern Korea. Associated minerals are calcite, nsutite, todorokite, and some undetermined manganese dioxide minerals. The name is for the mine, the first locality. The mineral and name were approved before publication by the Commission on New Minerals and Mineral Names, I.M.A.

• Tuberculosis and Respiratory Diseases
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• v.45 no.6
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• pp.1265-1276
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• 1998

Background : Nitric oxide(NO) is an endogenously produced free radical that plays an important role in regulating vascular tone, inhibition of platelet aggregation and white blood cell adhesion to endothelial cells, and host defense against infection. The highly reactive nature of NO with oxygen radicals suggests that it may either promote or reduce oxidant-induced cell injury in several biological pathways. Oxidant injury and interactions between pulmonary vascular endothelium and leukocytes are important in the pathogenesis of acute lung injury, including acute respiratory distress syndrome(ARDS). In ARDS, therapeutic administration of NO is a clinical condition providing exogenous NO in oxidant-induced endothelial injury. The role of exogenous NO from NO donor or the suppression of endogenous NO production was evaluated in oxidant-induced endothelial injury. Method : The oxidant injury in cultured rat lung microvascular endothelial cells(RLMVC) was induced by hydrogen peroxide generated from glucose oxidase(GO). Cell injury was evaluated by $^{51}$chromium($^{51}Cr$) release technique. NO donor, such as S-nitroso-N-acetylpenicillamine(SNAP) or sodium nitroprusside(SNP), was added to the endothelial cells as a source of exogenous NO. Endogenous production of NO was suppressed with N-monomethyl-L-arginine(L-NMMA) which is an NO synthase inhibitor. L-NMMA was also used in increased endogenous NO production induced by combined stimulation with interferon-$\gamma$(INF-$\gamma$), tumor necrosis factor-$\alpha$(TNF-$\alpha$), and lipopolysaccharide(LPS). NO generation from NO donor or from the endothelial cells was evaluated by measuring nitrite concentration. Result : $^{51}Cr$ release was $8.7{\pm}0.5%$ in GO 5 mU/ml, $14.4{\pm}2.9%$ in GO 10 mU/ml, $32.3{\pm}2.9%$ in GO 15 mU/ml, $55.5{\pm}0.3%$ in GO 20 mU/ml and $67.8{\pm}0.9%$ in GO 30 mU/ml ; it was significantly increased in GO 15 mU/ml or higher concentrations when compared with $9.6{\pm}0.7%$ in control(p < 0.05; n=6). L-NMMA(0.5 mM) did not affect the $^{51}Cr$ release by GO. Nitrite concentration was increased to $3.9{\pm}0.3\;{\mu}M$ in culture media of RLMVC treated with INF-$\gamma$ (500 U/ml), TNF-$\alpha$(150 U/ml) and LPS($1\;{\mu}g/ml$) for 24 hours ; it was significantly suppressed by the addition of L-NMMA. The presence of L-NMMA did not affect $^{51}Cr$ release induced by GO in RLMVC pretreated with INF-$\gamma$, TNF-$\alpha$ and LPS. The increase of $^{51}Cr$ release with GO(20 mU/ml) was prevented completely by adding 100 ${\mu}M$ SNAP. But the add of SNP, potassium ferrocyanate or potassium ferricyanate did not protect the oxidant injury. Nitrite accumulation was $23{\pm}1.0\;{\mu}M$ from 100 ${\mu}M$ SNAP at 4 hours in phenol red free Hanks' balanced salt solution. But nitrite was not detectable from SNP upto 1 mM The presence of SNAP did not affect the time dependent generation of hydrogen peroxide by GO in phenol red free Hanks' balanced salt solution. Conclusion : Hydrogen peroxide generated by GO causes oxidant injury in RLMVC. Exogenous NO from NO donor prevents oxidant injury, and the protective effect may be related to the ability to release NO. These results suggest that the exogenous NO may be protective on oxidant injury to the endothelium.