408 research outputs found

    Microbial biomass in relation to primary succession on arctic deglaciated moraines

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    Microbial biomass in arctic soil was examined in relation to a primary succession on arctic deglaciated moraines in Ny-Alesund, Svalbard (79°N, 12°E). Soil samples at four study sites representing different successional stages were collected at every 1cm depth from the soil surface to 3cm depth in early August 1995. Microbial biomass was measured with a substrate-induced respiration procedure. The microbial biomass was highest at the soil surface (0-1cm depth) in all successional stages, and decreased to a negligible amount at 3cm depth. Mean microbial biomass in 0-2cm layer increased from 0.06mgCg^ soil d. w. in the youngest site to 1.03mgC g^ soil d. w. in the oldest site, which is comparable to ecosystems in warmer regions. Throughout all successional stages, there was positive high correlation between soil carbon or nitrogen content and microbial biomass

    Soil respiration in a high arctic glacier foreland in Ny-Alesund, Svalbard

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    Soil respiration rates were measured in a successional glacier foreland in Ny-_lesund, Svalbard, and the amount of CO2 efflux during the plant-growing season was estimated using a simple regression model. Three study sites (Site 1, Site 2 and Site 3) were set up along with the primary succession in the deglaciated area of East Br_gger glacier in Ny-_lesund, Svalbard, Norway (79‹N 12‹E). Another study site, Site RB, was set up on a riverbed in the Bay River between Site 2 and Site 3. Soil respiration (SR), air temperature at 10 cm height (AT), soil surface temperature (SST) and soil temperature at 1 cm depth (ST) were measured at the four study sites with an open-airflow system using an infra-red gas analyzer from July to August, 1995. The mean soil respiration rate varied among the four sites: 6.2, 44, 63 and 3.7 mg CO2 m-2 h-1 at Site 1, Site 2, Site 3 and Site RB, respectively. These differences in the soil respiration rate among the four sites corresponded with the soil organic amount, microbial biomass, and root biomass. The soil respiration rate showed the best correlation with AT at Site 1, Site 2 and Site RB, and with ST at Site 3. The cumulative amount of CO2 efflux calculated using correlation equations obtained from the above relationships between SR and AT or ST was 5.8, 46, 69 and 3.3 g CO2 m-2 at Site 1, Site 2, Site 3 and Site RB, respectively, for two months (from July to August, 1995). These values were extremely low compared to those of warmer ecosystems, such as low-arctic tundra, temperate mixed forests, and tropical moist forests

    Exogenous surfactant instillation attenuates inflammatory response to acid-induced lung injury in rat

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    The present study was performed to investigate the role of exogenous surfactant on hydrochloric acid (HCL) - induced lung injury in rats. Six-week-old male Sprague-Dawley rats were anesthetized by intraperitoneal injection of pentobarbital sodium (40 mg/kg) and HCL (0.1 N, 2 mL/kg) or normal saline (NS, 2 mL/kg) was instilled into the trachea. Thirty minutes after HCL instillation, surfactant at a dose of 60 mg (=2 mL)/body or NS (2 mL) was instilled into the rat lungs. Animals in another experimental group were also treated with the same dose of surfactant supplement 2 hours after the first administration. Bronchoalveolar lavage fluid (BALF) was obtained 5 hours after HCL instillation. In BALF, increases in total nuclear cell counts, neutrophil counts, optical density at 412 nm as an indicator Of Pulmonary hemorrhage, neutrophil elastase activity, concentrations of albumin and cytokine-induced neutrophil chemoattractant (CINC) induced by HCL instillation were significantly attenuated by surfactant treatment. The wet-to-dry weight (W/D) ratio in the lung and partial oxygen tension (P-O2) were also estimated; surfactant treatment significantly attenuated the W/D ratio and improved deteriorated P-O2 induced by HCL Additional surfactant supplementation did not show further beneficial effects on HCL-induced lung injury compared with a single treatment. These results suggest that surfactant shows an anti-inflammatory effect on acid lung injury in rats but the beneficial effects may be dose limited.ArticlePULMONARY PHARMACOLOGY & THERAPEUTICS. 23(1):43-47 (2010)journal articl

    ICONE 17 -75179 Heat Transfer Experiments of Mini-Tube Bank

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    ABSTRACT Heat transfer and flow behavior in the mini rod bank were examined. The tubes are simulated with a 1 mm diameter nickel wire. The tube bank was composed of the 5×5 square-lattice array and the 5×5 staggered array. The tube banks were arranged in the flow channel of 30 mm wide or 15 mm wide, 15 mm high and 480 mm long. Water was used as the test fluid. A flow rate was varied in the range of the Reynolds number Re = uD/ν of 1 ~ 800, where D is the tube diameter. The approaching velocity of fluid in the channel was in the range of 0.0036 m/s ~ 0.68 m/s. Experiments were performed at atmospheric pressure. The measured heat transfer coefficients of the rows after the second row were lower than those of the first row and the difference between those increased as the Reynolds number was increased. The difference turned to decrease around Reynolds number = 50 in the 15 mm wide test section experiments of the square -lattice array and around Reynolds number = 200 in the 30 mm wide test section experiments of the staggered array. The heat transfer coefficients reached back to the first row value around Re = 400 in the former experiments. It was confirmed through the present results and the previous results that the heat transfer in the rear rows is deteriorated by the flow stagnation in the wake region of the preceding rod and the deterioration is recovered as the Reynolds number is increased since the wake region becomes disturbed

    Accumulation of Uroporphyrin I in Necrotic Tissues of Squamous Cell Carcinoma after Administration of 5-Aminolevulinic Acid

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    5-aminolevulinic acid (5-ALA)-induced protoporphyrin IX (PpIX) fluorescence is widely used for the intraoperative detection of malignant tumors. However, the fluorescence emission profiles of the accompanying necrotic regions of these tumors have yet to be determined. To address this, we performed fluorescence and high-performance liquid chromatography (HPLC) analyses of necrotic tissues of squamous cancer after 5-ALA administration. In resected human lymph nodes of metastatic squamous cell carcinoma, we found a fluorescence peak at approximately 620 nm in necrotic lesions, which was distinct from the PpIX fluorescence peak at 635 nm for viable cancer lesions. Necrotic lesions obtained from a subcutaneous xenograft model of human B88 oral squamous cancer also emitted the characteristic fluorescence peak at 620 nm after light irradiation: the fluorescence intensity ratio (620 nm/635 nm) increased with the energy of the irradiation light. HPLC analysis revealed a high content ratio of uroporphyrin I (UPI)/total porphyrins in the necrotic cores of murine tumors, indicating that UPI is responsible for the 620 nm peak. UPI accumulation in necrotic tissues after 5-ALA administration was possibly due to the failure of the heme biosynthetic pathway. Taken together, fluorescence imaging of UPI after 5-ALA administration may be applicable for the evaluation of tumor necrosis

    Prognostic value of metastin expression in human pancreatic cancer

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    <p>Abstract</p> <p>Background</p> <p><it>KiSS-1 </it>was identified as a metastasis-suppressing gene in melanoma cells. The <it>KiSS-1 </it>gene product (metastin) was isolated from human placenta as the ligand of GPR54, a G-protein-coupled receptor. The role of metastin and GPR54 in tumor progression is not fully understood.</p> <p>Methods</p> <p>We investigated the clinical significance of metastin and GPR54 expression in pancreatic cancer. We evaluated immunohistochemical expression of metastin and GPR54 in pancreatic ductal adenocarcinoma tissues obtained from 53 consecutive patients who underwent resection between July 2003 and May 2007 at Kyoto University Hospital. In 23 consecutive patients, the plasma metastin level was measured before surgery by enzyme immunoassay.</p> <p>Results</p> <p>Strong immunohistochemical expression of metastin was detected in 13 tumors (24.5%), while strong expression of GPR54 was detected in 30 tumors (56.6%). Tumors that were negative for both metastin and GPR54 expression were significantly larger than tumors that were positive for either metastin or GPR54 (p = 0.047). Recurrence was less frequent in patients who had metastin-positive tumors compared with those who had metastin-negative tumors (38.5% versus 70.0%, p = 0.04). Strong expression of metastin and GPR54 was significantly correlated with longer survival (p = 0.02). Metastin expression by pancreatic cancer was an independent prognostic factor for longer survival (hazard ratio, 2.1; 95% confidence interval, 1.1–4.7; p = 0.03), and the patients with a high plasma metastin level (n = 6) did not die after surgical resection.</p> <p>Conclusion</p> <p>Strong expression of metastin and GPR54 by pancreatic cancer is associated with longer survival. Metastin expression is an independent prognostic factor for the survival of pancreatic cancer patients. The plasma metastin level could become a noninvasive prognostic factor for the assessment of pancreatic cancer.</p

    Long-term clinical outcomes of 420 consecutive prostate cancer patients in a single institute.

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    This study was undertaken to reveal the trends of prostate cancer and the outcome of treatment modalities for each disease stage in patients in a single institute over a 10-year period. From January 1994 through December 2003, 420 consecutive patients with previously untreated and histologically confirmed prostate cancer were analyzed for annual distributions of disease stages and treatment modalities and for long-term clinical progression-free survival, prostate cancer-specific survival, and prostate-specific antigen (PSA) failure-free survival rates for each stage and treatment modality. Annual trends showed that the number of patients, especially those with clinically localized cancer, increased dramatically. The 5-year disease-specific survival rates for patients with clinically localized disease were 100 percent for all treatment modalities, including hormonal therapy alone. Patients with PSA levels less than 10 ng/ml showed an 81 percent 5-year PSA failure-free survival rate with radical prostatectomy. Stage C patients treated by surgery or radiation-based therapy with concomitant hormonal therapy obtained 93 percent and 100 percent cause-specific survival rates, respectively, and those treated by hormonal therapy alone showed a 79 percent rate. The number of patients with localized prostate cancer was increasing in this decade. While long-term hormonal therapy alone was highly efficient in controlling localized prostate cancer, radical therapies in conjunction with neo-adjuvant hormonal therapy produced better survival rates in cases of locally advanced disease.</p

    Research Evidence on High-Fat Diet-Induced Prostate Cancer Development and Progression

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    Although recent evidence has suggested that a high-fat diet (HFD) plays an important role in prostate carcinogenesis, the underlying mechanisms have largely remained unknown. This review thus summarizes previous preclinical studies that have used prostate cancer cells and animal models to assess the impact of dietary fat on prostate cancer development and progression. Large variations in the previous studies were found during the selection of preclinical models and types of dietary intervention. Subcutaneous human prostate cancer cell xenografts, such as LNCaP, LAPC-4, and PC-3 and genetic engineered mouse models, such as TRAMP and Pten knockout, were frequently used. The dietary interventions had not been standardized, and distinct variations in the phenotype were observed in different studies using distinct HFD components. The use of different dietary components in the research models is reported to influence the effect of diet-induced metabolic disorders. The proposed underlying mechanisms for HFD-induced prostate cancer were divided into (1) growth factor signaling, (2) lipid metabolism, (3) inflammation, (4) hormonal modulation, and others. A number of preclinical studies proposed that dietary fat and/or obesity enhanced prostate cancer development and progression. However, the relationship still remains controversial, and care should be taken when interpreting the results in a human context. Future studies using more sophisticated preclinical models are imperative in order to explore deeper understanding regarding the impact of dietary fat on the development and progression of prostate cancer

    Serum lipoprotein lipase mass: Clinical significance of its measurement

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    金沢大学大学院医学系研究科Lipoprotein lipase (LPL) is a lipolytic enzyme involved in catalyzing hydrolysis of triglycerides (TG) in chylomicrons and very low-density lipoprotein (VLDL) particles. Over the last decade, increasing attention has been paid to the clinical significance of measuring serum LPL protein mass without heparin injection to the study subjects. In earlier studies, this marker was utilized to classify LPL deficient subjects, which is an extremely rare metabolic disorder with a frequency of one in one million. Later, researchers paid more attention to the clinical significance of measuring this parameter in more common metabolic disorders. Studies have shown that pre-heparin plasma or serum LPL mass has significant relationships with serum lipids and lipoproteins, visceral fat area, insulin resistance, and even the development of coronary atherosclerosis in cross-sectional studies, although this might be a metabolic surrogate marker with almost no catalytic activities, which does not appear to be involved in catalyzing hydrolysis of TG in TG-rich lipoproteins. Recently, a prospective study has demonstrated that low serum LPL concentration predicts future coronary events. Taken together, we suggest that pre-heparin LPL mass in plasma or sera provide us with useful and important information on the development of metabolic disorders leading to atherosclerotic disease. © 2006 Elsevier B.V. All rights reserved
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