675 research outputs found

    SYNGAS PRODUCTION WITH A DUAL FLUIDIZED BED GASIFIER FOR POLYGENERATION

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    A pilot scale dual fluidized bed gasification system was developed for polygeneration with biomass. The gasification system is designed for supplying syngas for Fischer Tropsch (F-T) synthesis of bio-diesel and power generation with a syngas engine. Characteristics of biomass steam gasification were investigated in a lab scale bubbling fluidized bed, and hydrodynamics of a dual fluidized bed were investigated in a cold flow model. Based on the results from the lab scale test and cold flow model, a pilot scale dual fluidized bed gasifier was designed. In this paper, the developing process of the gasifier and preliminary results of system operation will be presented

    Downregulation of Protein Kinase CK2 Activity Facilitates Tumor Necrosis Factor-ฮฑ-Mediated Chondrocyte Death through Apoptosis and Autophagy

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    Despite the numerous studies of protein kinase CK2, little progress has been made in understanding its function in chondrocyte death. Our previous study first demonstrated that CK2 is involved in apoptosis of rat articular chondrocytes. Recent studies have suggested that CK2 downregulation is associated with aging. Thus examining the involvement of CK2 downregulation in chondrocyte death is an urgently required task. We undertook this study to examine whether CK2 downregulation modulates chondrocyte death. We first measured CK2 activity in articular chondrocytes of 6-, 21- and 30-month-old rats. Noticeably, CK2 activity was downregulated in chondrocytes with advancing age. To build an in vitro experimental system for simulating tumor necrosis factor (TNF)-ฮฑ-induced cell death in aged chondrocytes with decreased CK2 activity, chondrocytes were co-treated with CK2 inhibitors and TNF-ฮฑ. Viability assay demonstrated that CK2 inhibitors facilitated TNF-ฮฑ-mediated chondrocyte death. Pulsed-field gel electrophoresis, nuclear staining, flow cytometry, TUNEL staining, confocal microscopy, western blot and transmission electron microscopy were conducted to assess cell death modes. The results of multiple assays showed that this cell death was mediated by apoptosis. Importantly, autophagy was also involved in this process, as supported by the appearance of a punctuate LC3 pattern and autophagic vacuoles. The inhibition of autophagy by silencing of autophage-related genes 5 and 7 as well as by 3-methyladenine treatment protected chondrocytes against cell death and caspase activation, indicating that autophagy led to the induction of apoptosis. Autophagic cells were observed in cartilage obtained from osteoarthritis (OA) model rats and human OA patients. Our findings indicate that CK2 down regulation facilitates TNF-ฮฑ-mediated chondrocyte death through apoptosis and autophagy. It should be clarified in the future if autophagy observed is a consequence versus a cause of the degeneration in vivo

    Clinical and Radiological Manifestations of Osteogenesis Imperfecta Type V

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    We reviewed clinical manifestation of 12 patients from three Korean families. They showed mild to moderate bone fragility, and suggested an autosomal dominant inheritance pattern. Significant intrafamilial phenotype variability was obvious. Clinical, radiological, and histopathologic characteristics that distinguished this subtype from others include ossification of interosseous membrane of the forearm with radial head dislocation, hyperplastic callus formation, no evidence of type I collagenopathy and an abnormal histopathologic pattern. Severity of the interosseous membrane ossification was correlated with increasing age (p<0.01) and the radial head dislocation was thought to be a developmental problem rather than a congenital problem. Four children who had bisphosphonate treatment showed improved bone mineral density, radiological changes, and biochemical responses. Osteogenesis imperfecta type V was a distinctive subtype of osteogenesis imperfecta, which caused mild to moderate disability clinically

    Oxygen-deficient triple perovskites as highly active and durable bifunctional electrocatalysts for oxygen electrode reactions

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    Highly active and durable bifunctional oxygen electrocatalysts have been of pivotal importance for renewable energy conversion and storage devices, such as unitized regenerative fuel cells and metal-air batteries. Perovskite-based oxygen electrocatalysts have emerged as promising nonprecious metal bifunctional electrocatalysts, yet their catalytic activity and stability still remain to be improved. We report a high-performance oxygen electrocatalyst based on a triple perovskite, Nd1.5Ba1.5CoFeMnO9-delta (NBCFM), which shows superior activity and durability for oxygen electrode reactions to single and double perovskites. When hybridized with nitrogen-doped reduced graphene oxide (N-rGO), the resulting NBCFM/N-rGO catalyst shows further boosted bifunctional oxygen electrode activity (0.698 V), which surpasses that of Pt/C (0.801 V) and Ir/C (0.769 V) catalysts and which, among the perovskite-based electrocatalysts, is the best activity reported to date. The superior catalytic performances of NBCFM could be correlated to its oxygen defect rich structure, lower charge transfer resistance, and smaller hybridization strength between O 2p and Co 3d orbitals

    ACVR1 Gene Mutation in Sporadic Korean Patients with Fibrodysplasia Ossificans Progressiva

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    Fibrodysplasia ossificans progressiva (FOP; OMIM 135100) is a rare but extremely disabling genetic disorder of the skeletal system, and is characterized by the progressive development of ectopic ossification of skeletal muscles and subsequent joint ankylosis. The c.617G>A; p.R206H point mutation in the activin A type I receptor (ACVR1) gene has been reported to be a causative mutation of FOP. In the present study, mutation analysis of the ACVR1 gene was performed in 12 patients diagnosed or suspected to have FOP. All patients tested had a de novo heterozygous point mutation of c.617G>A; p.R206H in ACVR1. Mutation analysis confirmed a diagnosis of FOP in patients with ambiguous features, and thus, could be used for diagnostic purposes. Early confirmation through mutation analysis would allow medical professionals to advise on the avoidance of provoking events to delay catastrophic flare-ups of ectopic ossifications

    G-protein coupled receptor 64 (GPR64) acts as a tumor suppressor in endometrial cancer

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    Background Endometrial cancer is the most common gynecological cancer. G-protein coupled receptor 64 (GPR64) belongs to a family of adhesion GPCRs and plays an important role in male fertility. However, the function of GPR64 has not been studied in endometrial cancer. Our objective is to investigate the role of GPR64 in endometrial cancer. Methods We examined the levels of GPR64 in human endometrioid endometrial carcinoma by immunohistochemistry analysis. To determine a tumor suppressor role of GPR64 in endometrial cancer, we used a siRNA loss of function approach in human endometrial adenocarcinoma cell lines. Results GPR64 levels were remarkably lower in 10 of 21 (47.62%) of endometrial carcinoma samples compared to control. Depletion of GPR64 by siRNA transfection revealed an increase of colony formation ability, cell proliferation, cell migration, and invasion activity in Ishikawa and HEC1A cells. The expression of Connexin 43 (Cx43), a member of the large family of gap junction proteins, was reduced through activation of AMP-activated protein kinase (AMPK) in Ishikawa cells with GPR64-deficicy. Conclusions These results suggest that GPR64 plays an important tumor suppressor role in endometrial cancer.Grant numbers and sources of support: The design, data collection, data analysis, and data interpretation of this study were supported by Bio-industry Technology Development Program (IPET312060โ€“5), Ministry for Food, Agriculture, Forestry and Fisheries, Republic of Korea (to J.M.L.), and NIH R01 HD084478 (to J.W.J.). The analysis and interpretation of data and writing support of this manuscript were supported by Basic Science Research Program through the National Research Foundation of Korea (NRF-2016R1D1A1B03934346), Ministry of Education, Science and Technology, Republic of Korea (to J.Y.Y.) and Grant Number P50CA098258 from the National Cancer Institute (to R.R.B. and T.H.K.)

    The Relationship between the Presence of Chromosomal Instability and Prognosis of Squamous Cell Carcinoma of the Lung: Fluorescence in situ Hybridization Analysis of Paraffin-embedded Tissue from 47 Korean Patients

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    To evaluate the prognostic importance of chromosomal instability (CIN) in squamous cell carcinoma (SCC) of the lung, the relationship between CIN detected by fluorescence in situ hybridization (FISH) and survival in SCC patients was examined. Forty-seven surgical specimens of lung SCC were analyzed. To identify tumors with CIN, p16 and multi-target DNA FISH assays for c-myc, chromosome 6, EGFR, and chromosome 5 (LAVysion, Vysis) were performed on nuclei extracted from paraffin-embedded tumor tissues. Survival rates were compared in terms of age, T factor, N factor, CIN, and smoking status. A sample was defined as CIN-positive if at least four of the five chromosomes were positive. Among the 47 specimens, 9 (19%) were CIN-positive. The overall survival rate was 66%. Overall survival rates were estimated as 33.3% for CIN-positive patients and 76.7% for CIN-negative patients (Hazard ratio 3.47; 95% Confidence interval, 1.25-9.67; P=0.017). In multivariate analysis, the presence of CIN was a predictive factor for survival. CIN-positive based on FISH can be prognostic factor of lung SCC

    Diagnostic accuracy of a three-protein signature in women with suspicious breast lesions: a multicenter prospective trial

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    Background Mammography screening has been proven to detect breast cancer at an early stage and reduce mortality; however, it has low accuracy in young women or women with dense breasts. Blood-based diagnostic tools may overcome the limitations of mammography. This study assessed the diagnostic performance of a three-protein signature in patients with suspicious breast lesions. Findings This trial (MAST; KCT0004847) was a prospective multicenter observational trial. Three-protein signature values were obtained using serum and plasma from women with suspicious lesions for breast malignancy before tumor biopsy. Additionally, blood samples from women who underwent clear or benign mammography were collected for the assays. Among 642 participants, the sensitivity, specificity, and overall accuracy values of the three-protein signature were 74.4%, 66.9%, and 70.6%, respectively, and the concordance index was 0.698 (95% CI 0.656, 0.739). The diagnostic performance was not affected by the demographic features, clinicopathologic characteristics, and co-morbidities of the participants. Conclusions The present trial showed an accuracy of 70.6% for the three-protein signature. Considering the value of blood-based biomarkers for the early detection of breast malignancies, further evaluation of this proteomic assay is warranted in larger, population-level trials. This Multi-protein Assessment using Serum to deTermine breast lesion malignancy (MAST) was registered at the Clinical Research Information Service of Korea with the identification number of KCT0004847 (https://cris.nih.go.kr).This study was supported by the Bertis Inc. The funders had no role in the design and conduct of the study; collection, management, analysis, and interpretation of the data; preparation, review, or approval of the manuscript; and decision to submit the manuscript for publication
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