• Journal of Radiation Protection and Research
• /
• v.15 no.2
• /
• pp.27-39
• /
• 1990

Appreciable radiation exposures certainly were occurred in the reactor burn-up, the nuelear fall-out and the surroundings of nuclear installations with radioactive effluents. Therefore, radioactive nuclides is not only potentially hazardous to workers of nuclear power plants and related industrials, but also the wokers who handle radioactive nuclides in biochemical research and nuclear medicine diagnostics. And in the case of occurring the nuclear accidents, the early medical treatment of radiation injury should be necessary but little is established medical procedures to decontaminate the victims of internal contamination of radioactive nuclides in korea. Accordingly, to achieve the basic data for protective roles and medical treatment of radiation injury, the present studies were carrid out to evaluate the decontamination of uranium by the chemical drugs. The results observed were summarized as follows: 1. The combined treatmet group of sodium bicarbonate and saline with uranyl nitrate injection simultaneously and the dithiothreitol group that was administered 30 minutes after uranyl nitrate injection were increased significantly in the change of body weight than uranyl nitrate-only group (P<0.005). 2. All the experimental groups were increased the fluid intake and urine volume on the uranyl nitrate-induced acute renal failure. but the combined treatment group of sodium bicarbonate and saline with uranyl nitrate injection simultaneously and the dithiothreitol group that was administered 30 minutes after uranyl nitrate injection have the higher increment of fluid intake and urine volume (P<0.05). 3. When sodium bicarbonate and saline was treated with uranyl nitrate injection simultaneously. and dithiothreitol was administered 30 minutes after uranyl nitrate injection. there was significantly reduced in BUN concentration (P<0.01). 4. When dithiothreitol was administered 30 minutes after uranyl nitrate injection. there was reduced more significantly on the increment of serum creatinine concentration than that observed in uranyl nitrate-only group(P<0.01). but when the combined treatment of sodium bicarbonate and saline with uranyl nitrate simultaneously, there was still. albeit much less marked. decrease in serum creatinine concentration. 5. The sodium bicarbonate and saline was treated with uranyl nitrate simultaneously and dithiothreitol was administered at 30 minutes after uranyl nitrate were excreted markedly higher urine creatinine concentration than the uranyl nitrate-only group. 6. Uranyl nitrate has been used in experimental animals to produce hydropic degeneration and swelling of proximal tubules, disappearance of microvilli and brush border or necrosis in the kidney and centrilobular necrosis, congestion, and telangiectasia of the liver. When the sodium bicarbonate and saline was treated with uranyl nitrate simultaneously, and dithiothreitol was administered. 30 minutes after uranyl nitrate, there was more marked the protective effect than uranyl nitrate-only group. Finally, if the sodium bicarbonate and saline may administered as quickly as possible each time that some risk for internal contamination, with uranium, and dithiothreitol is administered 30 minutes after uranium contamination, there ameliorates the course of uranyl nitrate-induced acute renal failure.and this effect is assocciated with prevention of uranium (heavy metal)-induced alterations in BUN, serum creatinine, urine creatinine, fluid intake, urine volume and body weight.

• Tuberculosis and Respiratory Diseases
• /
• v.53 no.3
• /
• pp.294-308
• /
• 2002

Background : The cell-mediated immune response plays an important role in tuberculosis. After being activated by mycobacterial antigens, T lymphocytes express a high affinity receptor (IL-2R) for interleukin-2 (IL-2) on their own surface and release a soluble fraction of the IL-2 receptor (sIL-2R) from the cell membrane into the circulation. Neopterin is a metabolite of guanosine-triphosphate, which is produced by stimulated macrophages under the influence of IFN-$\gamma$ with a T lymphocyte origin. Therefore, the utility of sIL-2R, IFN-$\gamma$ and the neopterin levels as immunologic indices of the cell-mediated immune response and severity of disease in patients with pulmonary tuberculosis was assessed. Methods : The serum sIL-2R, IFN-$\gamma$ and neopterin levels were measured in 39 patients with pulmonary tuberculosis, 6 patients with tuberculous lymphadenitis prior to treatment and 10 healthy subjects. The serum and pleural sIL-2R, neopterin and ADA levels were measured in 22 patients with tuberculous pleurisy. The patients with pulmonary tuberculosis were divided into a mild, moderate and severe group according to the severity by ATS guidelines. To compare the results from these patients with those of the pretreatment levels, the sIL-2R, IFN-$\gamma$ and neopterin levels were measured in 36 of the 39 patients(1 patient, expired; 2 patients were referred to a sanitarium) with pulmonary tuberculosis after 2 months of treatment. Results : 1) the serum sIL-2R and IFN-$\gamma$ levels were elevated in patients with tuberculosis when compared to those of healthy subjects (p>0.05). The neopterin concentration in the serum was significantly lower in patients with pulmonary tuberculosis($2967{\pm}2132.8$ pg/ml) than in healthy controls($4949{\pm}1242.1$ pg/ml)(p<0.05). 2) In the pulmonary tuberculosis group, the serum sIL-2R and IFN-$\gamma$ levels were higher in patients with severe disease than those in patients with mild and moderate disease. However, the neopterin levels declined as the pulmonary tuberculosis became more severe (p<0.01). 3) The mean serum sIL-2R and IFN-$\gamma$ levels declined from $1071{\pm}1139.4$ U/ml to $1023{\pm}1920.9$ U/ml(p>0.05), $41{\pm}52.8$ pg/ml to $22{\pm}23.9$ gm/ml(p<0.05), respectively, after 2 month of treatment. The mean serum neopterin levels increased from $3158{\pm}2272.6$ pg/ml to $3737{\pm}2307.5$ pg/ml(p>0.05) after a 2 month of treatment. These findings were remarkable in the severe group of pulmonary tuberculosis with a clinical correlation. 4) In the patients with tuberculous pleurisy, the serum sIL-2R and ADA were significantly higher than those in the pleural fluid, However, the neopterin levels in the sera and pleural effusion were similar. Conclusion : On the basis of this study, sIL-2R, IFN-$\gamma$ and neopterin measurements may not only provide an insight into the present state of the cell-mediated immune response, but also serve as parameters monitoring of the prognosis of the disease, particularly in patients with severe pulmonary tuberculosis. In addition, an assay of the pleural sIL-2R levels might signal a stimulated local immunity including T cell activation in the tuberculous pleural effusion.

• Tuberculosis and Respiratory Diseases
• /
• v.51 no.4
• /
• pp.303-314
• /
• 2001

Background : Matrix metalioproteinase(MMP)-2 and MMP-9 have been known to play an important role in cell migration and the tissue remodeling process by type IV collagen lysis, a major component of the basement membrane. Intra-alveolar fibrosis, secondary to an injury to the basement membrane of the alveolar epithelial lining, is a major process in the pathogenesis of idiopathic pulmonary fibrosis(IPF). Therefore, MMP-2 and MMP-9 was hypothesized to play an important role in IPF pathogenesis. As a result, their level may reflect the activity or prognosis. Method : Forty one progressive IPF patients(age $59.82{\pm}1.73$ years, M:F=23:18), 16 patients with stable IPF for more than one year without therapy(age : $63.6{\pm}2.8$ years, M:F=13:3), and 7 normal controls were enrolled in this study. The MMP-2 and MMP-9 levels in the BAL fluid and alveolar macrophage conditioned media(AM-CM) were measured by zymography and the TIMP-1 level was measured by ELISA. Results : 1) The MMP-2 level in BALF was highest in the progressive IPF group ($1.36{\pm}0.28$) followed by the stable group ($0.46{\pm}0.13$) and the controls ($0.08{\pm}0.09$), which was statistically significant. The MMP-9 level of the IPF ($0.31{\pm}0.058$) and the stable group ($0.22{\pm}0.078$) were higher than that of the control group ($0.002{\pm}0.004$). In the AM-CM, only MMP-9 was detected, which was significantly higher in IPF group ($0.80{\pm}0.1O$) than in the control group($0.23{\pm}0.081$). The TIMP-1 level was also higher in both the IPF ($36.34{\pm}8.62\;{\mu}g/ml$) and stable group ($20.83{\pm}8.53\;{\mu}g/ml$) compared to the control group ($2.80{\pm}1.05\;{\mu}g/ml$) (p<0.05). 3) There was a correlation between the MMP-2 level in the BALF with the total cell number(r=0.298) and neutrophils(r=0.357) (p<0.05), and the MMP-9 level with the number of neutrophils (r=0.407) and lymphocytes (r=0.574)(p<0.05). The TIMP-1 level correlated with the total number of cell (r=0.338, p<0.05) and neutrophils(r=0.449, p=0.059). Conclusion : Both MMP and TIMP appear to play an important role in IPF pathogenesis, and their level may reflect the disease activity.

• Tuberculosis and Respiratory Diseases
• /
• v.43 no.4
• /
• pp.579-589
• /
• 1996

Background : Activation of neutrophil is critical for the clearance of microorganisms and toxic host mediators during sepsis. Unfortunately the activated neutrophil and its toxic byproducts can produce tissue injury and organ dysfunction. The leucocyte CD11/18 adhesion complex regulates neutrophil-endothelial cell adhesion, the first step in neutrophil migration to sites of injection and inflammation. To investigate the potential of neutrophil inhibition as a treatment strategy for sepsis, we evaluated the effects of monoclonal antibody against CD11b (MAb 1B6) in rats intrabronchial challenged with Escherichia coli. Methods : Animals were randomly assigned to receive monoclonal antibody against CD11b (1 mg/kg, sc) and bovine serum albumin(BSA, 1 mg/kg, sc) 6 hr before, at 0 and 6 hr after intrabronchial challenge of $20x10^9$ CFU/kg E. coli 0111. Animals were randomized to treat either 24, 60 or 90% oxygen after bacterial challenge and begining 4 hr after inoculation, all animals were received 100 mg/kg ceftriaxone qd for 3 days. Peripheral and alveolar neutrophil(by bronchoalveolar lavage) counts and lung injury parameters such as alveolar-arte rial $PO_2$ difference, wet to dry lung weight ratio and protein concentration of alveolar fluid were measured in survived rats at 12 hr and 96 hr. Results : Monoclonal antibody against CD11b decreased circulating and alveolar neutrophil especially more in 12 hr than in 96 hr The lung injury parameters of antibody-treated animals were not different from those of BSA-treated animals. but It was meaningless due to small number of survived animals. The early(6 hr) mortality rate was significantly increased in antibody-treated group(51%) compared to BSA-treated group(31%) (P=0.02) but late(from 12 hr to 72 hr) mortality rate was not different in antibody-treated group(44%) from BSA-treated group(36%) (P =0.089). Conclusion : Leucocyte CD11b/18 adhesion molecule is known to regulate neutrophil migration to the site of infection and inflammation. The monoclonal antibody against CD11b decreased alveolar neutrophil in rats with pulmonary sepsis and increased early mortality rate. Therefore, we can speculate that monoclonal antibody against CD11b blocks of alveolar recruitment of neutrophils, impairs host defense mechanism and increases early mortality rate of pulmonary sepsis in rat.

• Tuberculosis and Respiratory Diseases
• /
• v.42 no.4
• /
• pp.455-464
• /
• 1995

Background: Considering that both humoral and cell mediated immunities play an important role for human tuberculosis infection, enzyme-linked immunosorbent assay(ELISA) measurement of immunoglobulin G (IgG) antibody to mycobacterial antigens can be used for the serologic diagnosis of tuberculous pleural effusion. Method: We measured absorbance values of IgG antibodies to purified-protein-derivative (PPD) and lipoarabinomannan-B (LAM-B) in the pleural fluid (PF) and the serum in 40 tuberculous (TPE) and 19 nontuberculous pleural effusions (NTPE). Results: 1) The IgG antibodies to PPD and LAM-B were significantly (P<0.0005) higher in the PF and the serum of TPE compared to NTPE. 2) The IgG antibodies to PPD and LAM-B in the serum were higher than that in PF. 3) Significant correlations were found between pleural and serum IgG antibodies to PPD and LAM-B. 4) With a cutoff value for IgG antibody to PPD in the PF of 0.091, sensitivity was 55.0% and specificity 94.7% in the diagnosis of TPE. 5) With a cutoff value for IgG antibody to LAM-B in the PF of 0.337, sensitivity was 50.0% and specificity 94.7% in the diagnosis of TPE. 6) The seropositive rates in TPE were not related to PPD skin test status, the amount of PF and coexisting active pulmonary tuberculosis. Conclusion: The assay of IgG antibodies to PPD and LAM-B might be useful for the diagnosis of TPE. Our study suggests the mechanism of passive transfer of IgG antibodies to PPD and LAM-B from the serum to the PF through pleural tissue.

• Tuberculosis and Respiratory Diseases
• /
• v.45 no.6
• /
• pp.1236-1251
• /
• 1998

Background : TNF-$\alpha$ appears to be a central mediator of the host response to sepsis. While TNF-$\alpha$ is mainly considered a proinflammatory cytokine, it can also act as a direct cytotoxic cytokine. However, there are not so many studies about the relationship bet ween TNF-$\alpha$ level and lung injury severity in ALI, particularly regarding the case of ALI caused by direct lung injury such as diffuse pulmonary infection. Recently, a natural defense mechanism, known as the stress response or the heat shock response, has been reported in cellular or tissue injury reaction. There are a number of reports examining the protective role of pre-induced heat stress proteins on subsequent LPS-induced TNF-$\alpha$ release from monocyte or macrophage and also on subsequent LPS-induced ALI in animals. However it is not well established whether the stress protein synthesis such as HSP can be induced from rat alveolar macrophages by in vitro or in vivo LPS stimulation. Methods : We measured the level of TNF-$\alpha$, the percentage of inflammatory cells in bronchoalveolar lavage fluid, protein synthesis in alveolar macrophages isolated from rats at 1, 2, 3, 4, 6, 12, and 24 hours after intratracheal LPS instillation. We performed histologic examination and also obtained histologic lung injury index score in lungs from other rats at 1, 2, 3, 4, 6, 12, 24 h after intratracheal LPS instillation. Isolated non-stimulated macrophages were incubated for 2 h with different concentration of LPS (0, 1, 10, 100 ng/ml, 1, or 10 ${\mu}g/ml$). Other non-stimulated macrophages were exposed at $43^{\circ}C$ for 15 min, then returned to at $37^{\circ}C$ in 5% CO2-95% for 1 hour, and then incubated for 2 h with LPS (0, 1, 10, 100ng/ml, 1, or 10 ${\mu}g/ml$). Results : TNF-$\alpha$ levels began to increase significantly at 1 h, reached a peak at 3 h (P<0.0001), began to decrease at 6 h, and returned to control level at 12 h after LPS instillation. The percentage of inflammatory cells (neutrophils and alveolar macrophages) began to change significantly at 2 h, reached a peak at 6 h, began to recover but still showed significant change at 12 h, and showed insignificant change at 24 h after LPS instillation compared with the normal control. After LPS instillation, the score of histologic lung injury index reached a maximum value at 6 h and remained steady for 24 hours. 35 kDa protein band was newly synthesized in alveolar macrophage from 1 hour on for 24 hours after LPS instillation. Inducible heat stress protein 72 was not found in any alveolar macrophages obtained from rats after LPS instillation. TNF-$\alpha$ levels in supernatants of LPS-stimulated macro phages were significantly higher than those of non-stimulated macrophages(p<0.05). Following LPS stimulation, TNF-$\alpha$ levels in supernatants were significantly lower after heat treatment than in those without heat treatment (p<0.05). The inducible heat stress protein 72 was not found at any concentrations of LPS stimulation. Whereas the 35 kDa protein band was exclusively found at dose of LPS of 10 ${\mu}g/ml$. Conclusion : TNF-$\alpha$ has a direct or indirect close relationship with lung injury severity in acute lung injury or acute respiratory distress syndrome. In vivo and in vitro LPS stimulation dose not induce heat stress protein 72 in alveolar macrophages. It is likely that 35 kDa protein, synthesized by alveolar macrophage after LPS instillation, does not have a defense role in acute lung injury.

• Journal of Haehwa Medicine
• /
• v.8 no.2
• /
• pp.211-243
• /
• 2000

This study was performed to investigate the cause, symptom, treatment, medicine of Wei symptom through the literature of oriental and western medicine. The results obtained were as follows: 1. Wei symptom is the symptom that reveals muscle relaxation without contraction and muscle relaxation occures in the lower limb or upper limb, in severe case, leads to death. 2. Since the pathology and etiology of Wei symptom was first described as "pe-yeol-yeop-cho"(肺熱葉焦) in Hung Ti Nei Ching(黃帝內經), for generations most doctors had have accepted it. but after Dan Ge(丹溪), it had been classified into seven causes, damp-heat(濕熱), phlegm-damp(濕痰), deficiency of qi(氣虛), deficiency of blood(血虛), deficiency of yin(陰處), stagnant blood(死血), stagnant food(食積). Chang Gyeng Ag(張景岳) added the cause of deficiency of source qi(元氣). 3. The concept of "To treat Yangming, most of all"(獨治陽明) was emphasized in the treatment of Wei symptom and contains nourishment of middle warmer energy(補益中氣), clearance of yangming-damp-heat(淸化陽明濕熱). 4. Since Nei-ching era(內經時代), Wei and Bi symptom(痺症) is differenciated according to the existence of pain. After Ming era(明代) appeared theory of co-existence of Wei symptom and pain or numbness but they were accepted as a sign of Wei symptom caused by the pathological factor phelgm(痰), damp(濕), stagnancy(瘀). 5. In the western medical point of view, Wei symptom is like paraplegia, or tetraplegia. and according to the causative disease, it is accompanied by dysesthesia, paresthsia, pain. thus it is more recommended to use hwal-hyel-hwa-ae(活血化瘀) method considering damp-heat(濕熱), qi deficiency of spleen and stornach(脾胃氣虛) as pathological basis than to simply differenciate Wei and Bi symptom according to the existence of pain. 6. The cause of Gullian-Barre syndrome(GBS) is consist of two factors, internal and external. Internal factors include asthenia of spleen and stomach, and of liver and kidney. External factors include summur-damp(暑濕), damp-heat(濕熱), cold-damp(寒濕) and on the basis of "classification and treatment according to the symptom of Zang-Fu"(臟腑辨證論治), the cause of GBS is classified into injury of body fluid by lung heat(肺熱傷津), infiltration of damp-heat(濕熱浸淫), asthenia of spleen and kidney(脾腎兩虛), asthenia of spleen and stomach(脾胃虛弱), asthenia of liver and kidney (肝腎兩虛). 7. The cause of GBS is divided by according to the disease developing stage: Early stage include dryness-heat(燥熱), damp(濕邪), phlegm(痰濁), stagnant blood(瘀血), and major treatment is reducing of excess(瀉實). Late stage include deficiency of essence(精虛), deficiency with excess(虛中挾實), and essencial deficiency of liver and kidney(肝腎精不足) is major point of treatment. 8. Following is the herbal medicine of GBS according to the stage. In case of summur-damp(暑濕), chung-seu-iki-tang(淸暑益氣湯) is used which helps cooling and drainage of summer-damp(淸利暑濕), reinforcement of qi and passage of collateral channels(補氣通絡). In case of damp-heat, used kun-bo-hwan(健步丸), In case of cool-damp(寒濕), used 'Mahwang-buja-sesin-tang with sam-chul-tang'(麻黃附子細辛湯合蓼朮湯). In case of asthenia of spleen and kidney, used 'Sam-lyeng-baik-chul san'(蔘笭白朮散), In case of asthenia of liver and kidney, used 'Hojam-hwan'(虎潛丸). 9. Following is the herbal medicine of GBS according to the "classification and treatment according to the symptom of Zang-Fu"(臟腑辨證論治). In the case of injury of body fluid by lung heat(肺熱傷津), 'Chung-jo-gu-pae-tang'(淸燥救肺湯) is used. In case of 'infiltration of damp-heat'(濕熱浸淫), us-ed 'Yi-myo-hwan'(二妙丸), In case of 'infiltration of cool-damp'(寒濕浸淫), us-ed 'Yui-lyung-tang', In case of asthenia of spleen, used 'Sam-lyung-bak-chul-san'. In case of yin-deficiency of liver and kidney(肝腎陰虛), used 'Ji-bak-ji-hwang-hwan'(知柏地黃丸), or 'Ho-jam-hwan'(虎潛丸). 10. Cervical spondylosis with myelopathy is occuered by compression or ischemia of spinal cord. 11. The cause of cervical spondylosis with myelopathy consist of 'flow disturbance of the channel points of tai-yang'(太陽經兪不利), 'stagnancy of cool-damp'(寒濕凝聚), 'congestion of phlegm-damp stagnant substances'(痰濕膠阻), 'impairment of liver and kidney'(肝腎虛損). 12. In treatment of cervical spondylosis with myelopathy, are used 'Ge-ji-ga-gal-geun-tang-gagam'(桂枝加葛根湯加減), 'So-hwal-lack-dan-hap-do-hong-eum-gagam(小活絡丹合桃紅飮加減), 'Sin-tong-chuck-ue-tang-gagam(身痛逐瘀湯加減), 'Do-dam-tang-hap-sa-mul-tang-gagam'(導痰湯合四物湯加減), 'Ik-sin-yang-hyel-guen-bo-tang'(益腎養血健步湯加減), 'Nok-gakyo-hwan-gagam'(鹿角膠丸加減). 13. The cause of muscle dystropy is related with 'the impairement of vital qi'(元氣損傷), and 'impairement of five Zang organ'(五臟敗傷). Symptoms and signs are classified into asthenia of spleen and stomach, deficiency with excess, 'deficiency of liver and kidney'(肝腎不足) infiltration of damp-heat, 'deficiency of qi and blood'(氣血兩虛), 'yang deficiency of spleen and kidney'(脾腎陽虛). 14. 'Bo-jung-ik-gi-tang'(補中益氣湯), 'Gum-gang-hwan'(金剛丸), 'Yi-gong-san-hap-sam-myo-hwan'(異功散合三妙丸), 'Ja-hyel-yang-gun-tang'(滋血養筋湯), 'Ho-jam-hwan'(虎潛丸) are used for muscle dystropy. 15. The causes of myasthenia gravis are classified into 'insufficiency of middle warmer energy'(中氣不足), 'deficiency of qi and yin of spleen and kidney'(脾腎兩處), 'asthenia of qi of spleen'(脾氣虛弱), 'deficiency of qi and blood'(氣血兩虛), 'yang deficiency of spleen and kidney'(脾腎陽虛). 16. 'Bo-jung-ik-gi-tang-gagam'(補中益氣湯加減), 'Sa-gun-ja-tang-hap-gi-guk-yang-hyel-tang'(四君子湯合杞菊地黃湯), 'Sa-gun-ja-tang-hap-u-gyi-eum-gagam'(四君子湯合右歸飮加減), 'Pal-jin-tang'(八珍湯), 'U-gyi-eum'(右歸飮) are used for myasthenia gravis.

• Tuberculosis and Respiratory Diseases
• /
• v.47 no.3
• /
• pp.321-330
• /
• 1999

Background : Early diagnosis and proper antibiotic treatment are very important in the management of ventilator-associated pneumonia (VAP) because of its high mortality. Bronchoscopy with a protected specimen brush (PSB) has been considered the standard method to isolate the causative organisms of VAP. However, this method burdens consumer economically to purchase a PSB. Another useful method for the diagnosis of VAP is quantitative cultures of aspirated specimens through bronchoscopic bronchoalveolar lavage (BAL), for which the infusion of more than 120 m1 of saline has been recommended for adequate sampling of a pulmonary segment. However, occasionally it leads to deterioration of the patient's condition. We studied the diagnostic efficacy of minibronchoalveolar lavage (miniBAL), which retrieves only 25 ml of BAL fluid, in the isolation of causative organisms of VAP. Methods: We included 38 consecutive patients (41 cases) suspected of having VAP on the basis of clinical evidence, who had received antibiotics before the bronchoscopy. The two diagnostic techniques of PSB and miniBAL, which were performed one after another at the same pulmonary segment, 'were compared prospectively. The cut-off values for quantitative cultures to define causative bacteria of VAP were more than $10^3$ colony-forming units (cfu)/ml for PSB and more than $10^4$ cfu/ml for BAL. Results: The amount of instilled normal saline required to retrieve 25 ml of BAL fluid was $93{\pm}32 ml$ (mean${\pm}$SD). The detection rate of causative agents was 46.3% (19/41) with PSB and 43.9% (18/41) with miniBAL. The concordance rate of PSB and miniBAL in the bacterial culture was 85.4% (35/41). Although arterial blood oxygen saturation dropped significantly (p<0.05) during ($92{\pm}10%$) and 10 min after ($95{\pm}3%$) miniBAL compared with the baseline ($97{\pm}3%$), all except 3 cases were within normal ranges. The significantly elevated heart rate during ($l25{\pm}24$/min, p<0.05) miniBAL compared with the baseline ($1l1{\pm}22$/min) recovered again in 10 min after ($111{\pm}26$/min) miniBAL. Transient hypotension was developed during the procedure in two cases. The procedure was stopped in one case due to atrial flutter. Conclusion: MiniBAL is a safe and effective technique to detect the causative organisms of VAP.

• Tuberculosis and Respiratory Diseases
• /
• v.40 no.3
• /
• pp.236-249
• /
• 1993

Background: Among the injurious agents to which the lung airspaces are constantly exposed are reactive species of oxygen. It has been widely believed that reactive oxygen species may be implicated in the etiology of lung injuries. In order to elucidated how this oxidant causes lung cell injury, we investigated the effects of exogenous $H_2O_2$ on alveolar epithelial barrier characteristics. Methods: Rat type II alveolar epithelial cells were plated onto tissue culture-treated polycarbonate membrane filters. The resulting confluent monolayers on days 3 and 4 were mounted in a modified Ussing chamber and bathed on both sides with HEPES-buffered Ringer solution. The changes in short-circuit current (Isc) and monolayer resistance (R) in response to the exogenous hydroperoxide were measured. To determine the degree of cellular catalase participation in protection against $H_2O_2$ injury to the barrier, experiments were repeated in the presence of 20 mM aminotriazole (ATAZ, an inhibitor of catalase) in the same bathing fluid as the hydroperoxide. Results: These monolayers have a high transepithelial resistance (>2000 ohm-$cm^2$) and actively transport $Na^+$ from apical fluid. $H_2O_2$(0-100 mM) was then delivered to either apical or basolateral fluid. Resulting indicated that $H_2O_2$ decreased Isc and R gradually in dose-dependent manner. The effective concentration of apical $H_2O_2$ at which Isc (or R) was decreased by 50% at one hour ($ED_{50}$) was about 4 mM. However, basolateral $H_2O_2$ exposure led to $ED_{50}$ for Isc (and R) of about 0.04 mM. Inhibition of cellular catalase yielded $ED_{50}$ for Isc (and R) of about 0.4 mM when $H_2O_2$ was given apically, while $ED_{50}$ for basolateral exposure to $H_2O_2$ did not change in the presence of ATAZ. The rate of $H_2O_2$ consumption in apical and basolateral bathing fluids was the same, while cellualr catalase activity rose gradually with time in culture. Conclusion: Our data suggest that basolateral $H_2O_2$ may affect directly membrane component (e.g., $Na^+,\;K^+$-ATPase) located on the basolateral cell surface. Apical $H_2O_2$, on the other hand, may be largely degraded by catalase as it passes through the cells before reaching these membrane components. We conclude that alveolar epithelial barrier integrity as measured by Isc and R are compromised by $H_2O_2$ being relatively sensitive to basolateral (and insensitive to apical) $H_2O_2$.

• Journal of the Korean Geotechnical Society
• /
• v.27 no.10
• /
• pp.81-92
• /
• 2011

The rheological properties of Wyoming bentonites are strongly influenced by the size of particles, cation exchangeable capacity, arrangement and morphology of clay mineral. This paper presents the results of rheological investigations on the Wyoming bentonites aqueous dispersions: two types of particle flocculation were considered. For the Wyoming bentonite, 0g/L and 30g/L NaCl equivalent salinity were added in fresh and salt water to examine the rheological behavior. This paper examined the general rheological characteristics, compatibility of rheological models and correlation between soil structure and change in rheological properties of Wyoming bentonite caused by increasing salinity. From flow curves of bentonites hydrated with fresh water and salt water, the observed general flow behavior is very close to shear thinning with yield stress (or ideal Bingham fluid with yield stress and plastic viscosity). However, the change of shear stress at the same shear rate is clear, particularly for lower shear rate. Well-known rheological models are used to fit the data. There is a good agreement between rheological model and data: Carreau, Herschel-Bulkley and power-law for S=0g/L and bilinear, Herschel-Bulkley and power-law for S=30g/L. It may be due to the fact that the internal structural bonding (strong modification of particle-particle interactions from edge-to-edge and/or edge-to-face to face-to-face) in soil matrix is affected from the evolution of rheological properties with different salinities.