Distributed human computation framework for linked data co-reference resolution

Distributed Human Computation (DHC) is a technique used to solve computational problems by incorporating the collaborative effort of a large number of humans. It is also a solution to AI-complete problems such as natural language processing. The Semantic Web with its root in AI is envisioned to be a decentralised world-wide information space for sharing machine-readable data with minimal integration costs. There are many research problems in the Semantic Web that are considered as AI-complete problems. An example is co-reference resolution, which involves determining whether different URIs refer to the same entity. This is considered to be a significant hurdle to overcome in the realisation of large-scale Semantic Web applications. In this paper, we propose a framework for building a DHC system on top of the Linked Data Cloud to solve various computational problems. To demonstrate the concept, we are focusing on handling the co-reference resolution in the Semantic Web when integrating distributed datasets. The traditional way to solve this problem is to design machine-learning algorithms. However, they are often computationally expensive, error-prone and do not scale. We designed a DHC system named iamResearcher, which solves the scientific publication author identity co-reference problem when integrating distributed bibliographic datasets. In our system, we aggregated 6 million bibliographic data from various publication repositories. Users can sign up to the system to audit and align their own publications, thus solving the co-reference problem in a distributed manner. The aggregated results are published to the Linked Data Cloud

Lactobacillus acidophilus ameliorates H. pylori-induced gastric inflammation by inactivating the Smad7 and NFκB pathways

<p>Abstract</p> <p>Background</p> <p><it>H. pylori </it>infection may trigger Smad7 and NFκB expression in the stomach, whereas probiotics promote gastrointestinal health and improve intestinal inflammation caused by pathogens. This study examines if probiotics can improve <it>H. pylori</it>-induced gastric inflammation by inactivating the Smad7 and NFκB pathways.</p> <p>Results</p> <p>Challenge with <it>H. pylori </it>increased IL-8 and TNF-α expressions but not TGF-β1 in MKN45 cells. The RNA levels of Smad7 in AGS cells increased after <it>H. pylori </it>infection in a dose-dependent manner. A higher dose (MOI 100) of <it>L. acidophilus </it>pre-treatment attenuated the <it>H. pylori</it>-induced IL-8 expressions, but not TGF-β1. Such anti-inflammatory effect was mediated via increased cytoplasmic IκBα and depletion of nuclear NFκB. <it>L. acidophilus </it>also inhibited <it>H. pylori</it>-induced Smad7 transcription by inactivating the Jak1 and Stat1 pathways, which might activate the TGF-β1/Smad pathway. <it>L. acidophilus </it>pre-treatment ameliorated IFN-γ-induced Smad7 translation level and subsequently reduced nuclear NF-κB production, as detected by western blotting.</p> <p>Conclusions</p> <p><it>H. pylori </it>infection induces Smad7, NFκB, IL-8, and TNF-α production <it>in vitro</it>. Higher doses of <it>L. acidophilus </it>pre-treatment reduce <it>H. pylori</it>-induced inflammation through the inactivation of the Smad7 and NFκB pathways.</p

Etiology and Treatment of Childhood Peptic Ulcer Disease in Taiwan: A Single Center 9-Year Experience

Background/PurposePeptic ulcer disease (PUD) in children is relatively rare as compared with adults. This study aimed to assess the etiology, clinical and histological characteristics, and treatment of PUD in children.MethodsAll children aged < 18 years with an endoscopic diagnosis of PUD were enrolled in a tertiary referral center. The demographic data, clinical, endoscopic, and histological findings were compared between patients with different causes of PUD.ResultsFrom 1234 endoscopic examinations, 67 (5.4%) children (median age, 11.4 years) with gastric ulcer (GU; n = 27) or duodenal ulcer (DU; n = 40) were included. Thirty-two (47.7%) of them had Helicobacter pylori infection and 11 (16.5%) had previous use of non-steroidal anti-inflammatory drugs (NSAIDs). Non-H. pylori, non-NSAID PUD was found in 24 (35.8%) patients. Children with H. pylori-related PUD had a significantly higher mean age, antral chronic inflammatory score, rate of familial PUD, and presence of DU and nodular gastritis than those with NSAID-related and non-H. pylori, non-NSAID PUD (p < 0.01). In contrast, children with NSAID-related PUD had a higher rate of upper gastrointestinal bleeding, associated with acute febrile disease, than those with H. pylori-related and non-H. pylori, non-NSAID PUD (p < 0.05). All but two patients with non-H. pylori, non-NSAID PUD were disease free after H. pylori eradication and proton pump inhibitor treatment for 1–2 months.ConclusionIn children, H. pylori-related PUD is associated with familial peptic ulcer and the presence of DU. However, short-term NSAID use is correlated highly with GU. The outcome of childhood PUD is good

The morphology of diaphragmatic defects in hepatic hydrothorax: Thoracoscopic finding

BackgroundUntil now, the pathophysiology of hepatic hydrothorax has been moot. We discuss (on the basis of gross videothoracoscopy findings in 11 cases and the literature) the pathogenesis and clinical presentation of this complex condition.MethodsWe prospectively studied 11 patients (age, 31–73 years; 6 men and 5 women) with refractory hepatic hydrothorax (Child-Pugh class B-C) who underwent thoracoscopic repair of diaphragmatic defects. The diaphragmatic defects were examined intraoperatively.ResultsThe diaphragmatic defects stemming from hepatic hydrothorax were classified into 4 morphologic types: type I, no obvious defect (1 patient); type II, blebs lying on the diaphragm (4 patients); type III, broken defects (fenestrations) in the diaphragm (8 patients); and type IV, multiple gaps in the diaphragm (1 patient). The type of diaphragmatic defect did not correlate with the volume occupied by the pleural effusion in the preoperative chest radiograms.ConclusionsThe finding of this study allowed hepatic hydrothorax pathophysiology to be directly visualized, and further studies concerning the treatment of hepatic hydrothorax might be based on these mechanisms

Impact of body-mass factors on setup displacement in patients with head and neck cancer treated with radiotherapy using daily on-line image guidance

BACKGROUND: To determine the impact of body-mass factors (BMF) before radiotherapy and changes during radiotherapy on the magnitude of setup displacement in patients with head and neck cancer (HNC). METHODS: The clinical data of 30 patients with HNC was analyzed using the alignment data from daily on-line on-board imaging from image-guided radiotherapy. BMFs included body weight, body height, and the circumference and bilateral thickness of the neck. Changes in the BMFs during treatment were retrieved from cone beam computed tomography at the 10th and 20th fractions. Setup errors for each patient were assessed by systematic error (SE) and random error (RE) through the superior-inferior (SI), anterior-posterior (AP), and medial-lateral (ML) directions, and couch rotation (CR). Using the median values of the BMFs as a cutoff, the impact of the factors on the magnitude of displacement was assessed by the Mann–Whitney U test. RESULTS: A higher body weight before radiotherapy correlated with a greater AP-SE (p = 0.045), SI-RE (p = 0.023), and CR-SE (p = 0.033). A longer body height was associated with a greater SI-RE (p = 0.002). A performance status score of 1 or 2 was related to a greater AP-SE (p = 0.043), AP-RE (p = 0.015), and SI-RE (p = 0.043). Among the ratios of the BMFs during radiotherapy, the values at the level of mastoid tip at the 20(th) fraction were associated with greater setup errors. CONCLUSIONS: To reduce setup errors in patients with HNC receiving RT, the use of on-line image-guided radiotherapy is recommended for patients with a large body weight or height, and a performance status score of 1–2. In addition, adaptive planning should be considered for those who have a large reduction ratio in the circumference (<1) and thickness (<0.94) over the level of the mastoid tip during the 20(th) fraction of treatment

Aorta Fluorescence Imaging by Using Confocal Microscopy

The activated leukocyte attacked the vascular endothelium and the associated increase in VEcadherin number was observed in experiments. The confocal microscopic system with a prism-based wavelength filter was used for multiwavelength fluorescence measurement. Multiwavelength fluorescence imaging based on the VEcadherin within the aorta segment of a rat was achieved. The confocal microscopic system capable of fluorescence detection of cardiovascular tissue is a useful tool for measuring the biological properties in clinical applications

Group Signatures and Accountable Ring Signatures from Isogeny-based Assumptions

Group signatures are an important cryptographic primitive providing both anonymity and accountability to signatures. Accountable ring signatures combine features from both ring signatures and group signatures, and can be directly transformed to group signatures. While there exists extensive work on constructing group signatures from various post-quantum assumptions, there has not been any using isogeny-based assumptions. In this work, we propose the first construction of isogeny-based group signatures, which is a direct result of our isogeny-based accountable ring signature. This is also the first construction of accountable ring signatures based on post-quantum assumptions. Our schemes are based on the decisional CSIDH assumption (D-CSIDH) and are proven secure under the random oracle model (ROM)

Proteome profiling of cadmium-induced apoptosis by antibody array analyses in human bronchial epithelial cells

Protein array technology is a powerful platform for the simultaneous determination of the expression levels of a number of proteins as well as post-translational modifications such as phosphorylation. Here, we screen and report for the first time, the dominant signaling cascades and apoptotic mediators during the course of cadmium (Cd)-induced cytotoxicity in human bronchial epithelial cells (BEAS-2B) by antibody array analyses. Proteins from control and Cd-treated cells were captured on Proteome Profiler™ Arrays for the parallel determination of the relative levels of protein phosphorylation and proteins associated with apoptosis. Our results indicated that the p38 MAPK- and JNK-related signal transduction pathways were dramatically activated by Cd treatment. Cd potently stimulates the phosphorylations of p38α (MAPK14), JNK1/2 (MAPK8/9), and JUN; while the phosphorylations of Akt1, ERK1/2 (MAPK3/1), GSK3β, and mTOR were suppressed. Moreover, there was an induction of proapoptotic protein BAX, release of cytochrome c (CYCS) from mitochondria, activation of caspase-3/9 (CASP3/9); as well as decreased expression of cell cycle checkpoint proteins (TP53, p21, and p27) and several inhibitors of apoptosis proteins (IAPs) [including cIAP-1/2 (BIRC2/3), XIAP (BIRC4), and survivin (BIRC5)]. Pretreatment of cells with the thiol antioxidant glutathione or p38 MAPK/JNK inhibitors before Cd treatment effectively abrogated ROS activation of p38 MAPK/JNK pathways and apoptosis-related proteins. Taken together, our results demonstrate that Cd causes oxidative stress-induced apoptosis; and the p38 MAPK/JNK and mitochondrial pathways are more importantly participated for signal transduction and the induction of apoptosis in Cd-exposed human lung cells.published_or_final_versio