• Korean Journal of Soil Science and Fertilizer
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• v.45 no.2
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• pp.272-279
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• 2012

In order to effectively treat livestock wastewater in constructed wetlands by natural purification method, removal velocities of pollutants under different injection methods in constructed wetlands were investigated. The removal velocities of chemical oxygen demand (COD), suspended solid (SS), T-N and T-P by continuous injection method were slightly rapid than those by intermittent injection method in full-scale livestock wastewater treatment plant. The removal velocity (K; $day^{-1}$) of COD by continuous injection method was $0.38\;d^{-1}$ for $1^{st}$ bed, $0.13\;d^{-1}$ for $2^{nd}$ bed, $0.17\;d^{-1}$ for $3^{rd}$ bed, $0.05\;d^{-1}$ for $4^{th}$ bed and $0.17\;d^{-1}$ for $5^{th}$ bed. The removal velocities (K; $day^{-1}$) of COD in $1^{st}$, $2^{nd}$, $3^{rd}$, $4^{th}$ and $5^{th}$ beds by intermittent injection method were $0.210\;d^{-1}$, $0.086\;d^{-1}$, $0.222\;d^{-1}$, $0.053\;d^{-1}$ and $0.137\;d^{-1}$, respectively. The removal velocity (K; $day^{-1}$) of SS by continuous injection method was $0.750\;d^{-1}$ for $1^{st}$ bed, $0.108\;d^{-1}$ for $2^{nd}$ bed, $0.120\;d^{-1}$ for $3^{rd}$ bed, $0.086\;d^{-1}$ for $4^{th}$ bed and $0.292\;d^{-1}$ for $5^{th}$ bed. The removal velocities (K; $day^{-1}$) of SS in $1^{st}$, $2^{nd}$, $3^{rd}$, $4^{th}$ and $5^{th}$ beds by intermittent injection method were $0.485\;d^{-1}$, $0.056\;d^{-1}$, $0.174\;d^{-1}$, $0.081\;d^{-1}$ and $0.227\;d^{-1}$, respectively. The removal velocity (K; $day^{-1}$) of T-N by continuous injection method was $0.361\;d^{-1}$ for $1^{st}$ bed, $0.121\;d^{-1}$ for $2^{nd}$ bed, $109\;d^{-1}$ for $3^{rd}$ bed, $0.047\;d^{-1}$ for $4^{th}$ bed and $0.155\;d^{-1}$ for $5^{th}$ bed. The removal velocities (K; $day^{-1}$) of T-N in $1^{st}$, $2^{nd}$, $3^{rd}$, $4^{th}$ and $5^{th}$ beds by intermittent injection method were $0.235\;d^{-1}$, $0.071\;d^{-1}$, $0.171\;d^{-1}$, $0.058\;d^{-1}$ and $0.126\;d^{-1}$, respectively. The removal velocity (K; $day^{-1}$) of T-P by continuous injection method was $0.803\;d^{-1}$ for $1^{st}$ bed, $0.084\;d^{-1}$ for $2^{nd}$ bed, $0.076\;d^{-1}$ for $3^{rd}$ bed, $0.118\;d^{-1}$ for $4^{th}$ bed and $0.301\;d^{-1}$ for $5^{th}$ bed. The removal velocities (K; $day^{-1}$) of T-P in $1^{st}$, $2^{nd}$, $3^{rd}$, $4^{th}$ and $5^{th}$ beds by intermittent injection method were $0.572\;d^{-1}$, $0.049\;d^{-1}$, $0.090\;d^{-1}$, $0.112\;d^{-1}$ and $0.222\;d^{-1}$, respectively.

• Journal of Chest Surgery
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• v.39 no.12 s.269
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• pp.879-890
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• 2006

Background: The dysfunction of multiple organs is found to be caused by reactive oxygen species as a major modulator of microvascular injury after hemorrhagic shock. Hemorrhagic shock, one of many causes inducing acute lung injury, is associated with increase in alveolocapillary permeability and characterized by edema, neutrophil infiltration, and hemorrhage in the interstitial and alveolar space. Aggressive and rapid fluid resuscitation potentially might increased the risk of pulmonary dysfunction by the interstitial edema. Therefore, in order to improve the pulmonary dysfunction induced by hemorrhagic shock, the present study was attempted to investigate how to reduce the inflammatory responses and edema in lung. Material and Method: Male Sprague-Dawley rats, weight 300 to 350 gm were anesthetized with ketamine(7 mg/kg) intramuscular Hemorrhagic Shock(HS) was induced by withdrawal of 3 mL/100 g over 10 min. through right jugular vein. Mean arterial pressure was then maintained at $35{\sim}40$ mmHg by further blood withdrawal. At 60 min. after HS, the shed blood and Ringer's solution or 5% albumin was infused to restore mean carotid arterial pressure over 80 mmHg. Rats were divided into three groups according to rectal temperature level($37^{\circ}C$[normothermia] vs $33^{\circ}C$[mild hypothermia]) and resuscitation fluid(lactate Ringer's solution vs 5% albumin solution). Group I consisted of rats with the normothermia and lactate Ringer's solution infusion. Group II consisted of rats with the systemic hypothermia and lactate Ringer's solution infusion. Group III consisted of rats with the systemic hypothermia and 5% albumin solution infusion. Hemodynamic parameters(heart rate, mean carotid arterial pressure), metabolism, and pulmonary tissue damage were observed for 4 hours. Result: In all experimental groups including 6 rats in group I, totally 26 rats were alive in 3rd stage. However, bleeding volume of group I in first stage was $3.2{\pm}0.5$ mL/100 g less than those of group II($3.9{\pm}0.8$ mL/100 g) and group III($4.1{\pm}0.7$ mL/100 g). Fluid volume infused in 2nd stage was $28.6{\pm}6.0$ mL(group I), $20.6{\pm}4.0$ mL(group II) and $14.7{\pm}2.7$ mL(group III), retrospectively in which there was statistically a significance between all groups(p<0.05). Plasma potassium level was markedly elevated in comparison with other groups(II and III), whereas glucose level was obviously reduced in 2nd stage of group I. Level of interleukine-8 in group I was obviously higher than that of group II or III(p<0.05). They were $1.834{\pm}437$ pg/mL(group I), $1,006{\pm}532$ pg/mL(group II), and $764{\pm}302$ pg/mL(group III), retrospectively. In histologic score, the score of group III($1.6{\pm}0.6$) was significantly lower than that of group I($2.8{\pm}1.2$)(p<0.05). Conclusion: In pressure-controlled hemorrhagic shock model, it is suggested that hypothermia might inhibit the direct damage of ischemic tissue through reduction of basic metabolic rate in shock state compared to normothermia. It seems that hypothermia should be benefit to recovery pulmonary function by reducing replaced fluid volume, inhibiting anti-inflammatory agent(IL-8) and leukocyte infiltration in state of ischemia-reperfusion injury. However, if is considered that other changes in pulmonary damage and inflammatory responses might induce by not only kinds of fluid solutions but also hypothermia, and that the detailed evaluation should be study.

• 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. ($12\%$).

• Tuberculosis and Respiratory Diseases
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• v.41 no.1
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• pp.1-10
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• 1994

Background: Patients with mitral stenosis(MS) have been demonstrated to have a variable degree of pulmonary dysfunction and exercise impairment. The hemodynamic changes of MS can be reversed after percutaneous mitral balloon valvuloplasty(PMV), but the extent and time course of the imporvement in pulmonary function and exercise capacity are not defined. Methods: In order to investigate the early(3 weeks or less)and late(3 months or more) effects of PMV on pulmonary function and determine if the pulmonary dysfunction is reversible even in patients with moderate to severe pulmonary hypertension, we performed the spirometry, measurements of diffusing capacity and lung volumes, and incremental exercise tests in patients with MS before and after PMV. Results: In 46 patients with MS(age: $40{\pm}12$years, male to female ratio: 1:2, mitral valve area: $0.8{\pm}0.2cm^2$) there was a significant increase in FVC(P<0.0025), $FEV_1$(P<0.001), $FEF_{25-75%}$(P<0.001, $FEF_{50%}$(P<0.001), PEF(P<0.0005), MVV(P<0.005), $\dot{V}O_2$max (P<0.0001), and AT(P<0.0001) after average 10 days of PMV. Also there was a significant decrease in DLco(P<0.0001) and DL/VA(P<0.0001). At later($5{\pm}2$months) follow-up in 11 patients, there was no further improvement in any parameters of pulmonary function and exercise test. Twenty nine patients with sinus rhythm were divided into 16 patients with pulmonary arterial pressure(PAP) more than 35mmHg and/or tricuspid regurgitation grade n or more(group A) and 13 patients with PAP less than 35mmHg(group B). Group A Patients had significantly lower FVC(P<0.001), $FEV_1$(P<0.001), DLco(P<0.05), $\dot{V}O_2$ max(P<0.025) and mitral valve area(P<0.025) than group B patients. Group A patients after PMV, showed significant increase in FVC(P<0.001), maximum $O_2$ pulse(P<0.00001) and $\dot{V}O_2$ max(P<0.00025). Both group showed an increase in AT(P<0.0001, P<0.005), but group A showed greater decrease in $\dot{V}E/\dot{V}O_2$ and $\dot{V}E/\dot{V}CO_2$ both at AT(P<0.001, P<0.001) and $\dot{V}O_2$ max(P<0.0001, P<0.0001) after PMV compared with group B. Conclusion: These data suggest that patients with MS can show increased pulmonary function and exercise performance within 1 month after PMV. Patients with moderate to severe pulmonary hypertension had a significant increase in exercise performance compared with those with mild to no pulmonary hypertension and it is thought to be related to a significat decrease of ventilation for a given oxygen consumption at maximum exercise.

• Proceedings of the KOR-BRONCHOESO Conference
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• 1972.03a
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• pp.6-7
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• 1972

The air pollutants can be classified into the irritant gas and the asphixation gas, and the irritant gas is closely related to the otorhinolaryngological diseases. The common irritant gases are nitrogen oxides, sulfur oxides, hydrogen carbon compounds, and the potent and irritating PAN (peroxy acyl nitrate) which is secondarily liberated from photosynthesis. Those gases adhers to the mucous membrane to result in ulceration and secondary infection due to their potent oxidizing power. 1. Sulfur dioxide gas Sulfur dioxide gas has the typical characteristics of the air pollutants. Because of its high solubility it gets easily absorbed in the respiratory tract, when the symptoms and signs by irritation become manifested initially and later the resistance in the respiratory tract brings central about pulmonary edema and respiratory paralysis of origin. Chronic exposure to the gas leads to rhinitis, pharyngitis, laryngitis, and olfactory or gustatory disturbances. 2. Carbon monoxide Toxicity of carbon monoxide is due to its deprivation of the oxygen carrying capacity of the hemoglobin. The degree of the carbon monoxide intoxication varies according to its concentration and the duration of inhalation. It starts with headache, vertigo, nausea, vomiting and tinnitus, which can progress to respiratory difficulty, muscular laxity, syncope, and coma leading to death. 3. Nitrogen dioxide Nitrogen dioxide causes respiratory disturbances by formation of methemoglobin. In acute poisoning, it can cause pulmonary congestion, pulmonary edema, bronchitis, and pneumonia due to its strong irritation on the eyes and the nose. In chronic poisoning, it causes chronic pulmonary fibrosis and pulmonary edema. 4. Ozone It has offending irritating odor, and causes dryness of na sopharyngolaryngeal mucosa, headache and depressed pulmonary function which may eventually lead to pulmonary congestion or edema. 5. Smog The most outstanding incident of the smog occurred in London from December 5 through 8, 1952, because of which the mortality of the respiratory diseases increased fourfold. The smog was thought to be due to the smoke produced by incomplete combustion and its byproduct the sulfur oxides, and the dust was thought to play the secondary role. In new sense, hazardous is the photochemical smog which is produced by combination of light energy and the hydrocarbons and oxidant in the air. The Yonsei University Institute for Environmental :pollution Research launched a project to determine the relationship between the pollution and the medical, ophthalmological and rhinopharyngological disorders. The students (469) of the "S" Technical School in the most heavily polluted area in Pusan (Uham Dong district) were compared with those (345) of "K" High School in the less polluted area. The investigated group had those with subjective symptoms twice as much as the control group, 22.6% (106) in investigated group and 11.3% (39) in the control group. Among those symptomatic students of the investigated group. There were 29 with respiratory symptoms (29%), 22 with eye symptoms (21%), 50 with stuffy nose and rhinorrhea (47%), and 5 with sore thorat (5%), which revealed that more than half the students (52%) had subjective symptoms of the rhinopharyngological aspects. Physical examination revealed that the investigated group had more number of students with signs than those of the control group by 10%, 180 (38.4%) versus 99 (28.8%). Among the preceding 180 students of the investigated group, there were 8 with eye diseases (44%), 1 with respiratory disease (0.6%), 97 with rhinitis (54%), and 74 with pharyngotonsillitis (41%) which means that 95% of them had rharygoical diseases. The preceding data revealed that the otolaryngological diseases are conspicuously outnumbered in the heavily polluted area, and that there must be very close relationship between the air pollution and the otolaryngological diseases, and the anti-pollution measure is urgently needed.

• 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.

• 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.